Are we more attracted to people of the same ethnicity? Are humans more attracted to people from their own ethnic groups? I ask this because most of the time people have relationships with people of their own ethnicity, and I wonder if it's purely social, or if there's more behind it.

The answer in extreme brief is yes.  Only about 9% of whites and 16% of blacks engage in interracial marriage in the U.S.

But really this deserves a fuller discussion.

The predominant pattern of mate selection in human beings is to marry within their ethnic group.  I say 'ethnic group' rather than 'race' because 'race' has no strong scientific definition. Racial groups as usually understood have about the same genetic variance as the overall species.  I need to point out here that races can have a strong geographical point of origin and thus races can in some cases be genetically identified, but these correlate poorly often with, say health risks or other clinical data.

Because its clear that interracial marriages are on the rise in the US, mating choices are often argued to be socially defined preferences.  Social attitudes affect men and women differently and different cultures too, as tracked by regional differences. Not the least is a limit of opportunities.  Being comfortable with people from other cultures or who simply look different.

Interestingly, Women at least in American studies are much more likely to state a same-race preference (see p17), while men are likely to demur from stating a preference, but act out a bias unconsciously, making both genders equally biased.

As mentioned in the comments by @AliceD, Mating preferences as described in traditional population biology are adapted from availability.  That's to say people don't meet because of ethnic boundaries such as geography, socioeconomic or social strata. Then there are socialized preferences.  I.e. growing up we are imprinted by the sorts of people we see, which can create preferences later in life.

Lastly there may be genetically conveyed preferences. The human race has been spreading out over the past 200,000 years or so.  That's a pretty small amount of time.

There are cases where such mating preferences have evolved.  There are 17 species of arctic penguins, species caused by migration around the globe.  Each species can actually mate with others nearby, but where the penguins met at the far end of the globe, the species do not mate because they have been separated for so long they have diverged.

But speciation events can take millions of years.  Its clear that human beings from the far corners of the globe can produce offspring - we are one species.  It seems as if we are only a fraction of the way towards two neighboring penguin species in the example above.  There doesn't seem to be any evidence that we are genetically predisposed to ethinic self mating.

Only by way of example (not to offend anyone!) you can choose an ethnic group which has divergent behavior and try to get an estimate of how big a role the social context plays.  Looking at the jewish community we see that 47% of jewish people have married out of group in recent statistics.  They are thinly distributed over a wide geographical region and availability is high for out-group marriage.  All this while orthodox jews have a practically non-existent out-group marriage rate. Not judging here, but only for illustrative purposes we can guess that social attitudes and behaviors are playing a large role here.

As and endnote, I'd also like to point out that since whites are about 50% of the US population and african americans are about 10%, the percentages not so disparate as they seem - all things being equal the average person one meets in the US is white.  For caucasians, approximately 50% of the population the average interracial marriage rate with no racial biases is is 50%.  For blacks its 90%.  Again, just using random shuffling for statistical point of view.


The probability of indirect human fertilization (follow-up) This question is a follow-up to
this one.

I've been wondering how small that probability is. As we all know, "safe" sex, that is (correctly) using a condom and all that, isn't perfectly safe. So, in order to put this question into perspective, I'd like to know which one (safe sex or indirect insemination) has the greater chance to lead to impregnation. In other words, can you explain the probability of this scenario in terms a layman like me can understand?

Thanks in advance!

Safer sex techniques are more risky.  Perfect condom use is associated with around a 2% pregnancy rate within a year.  According to that, even sterilization has a 0.1% (male) or 0.5% (female) rate.  Combining techniques is, of course, safer.  "Indirect," as you proposed in the other question, will border on an infinitesimally small chance, as answered there.


Relationship of bases in a gene to amino acids One of my study questions for a biology test was:

A gene contains 1200 bases. How many codons will be on the mRNA immediately after transcription?

My initial answer was 400 codons, because 1200 bases = 1200 nucleotides and 1200/3 = 400. But since DNA is double helix, and only one of the two strands is used in mRNA creation, would only 600 bases be used instead of the full 1200?

Assuming that all 1200 bases in the gene code for mRNA, then 1200/3 = 400 is the correct calculation.

It's important to understand that a gene will only ever be transcribed from one strand of double-stranded DNA. Think about it mechanistically - first, DNA is transcribed to RNA by a polymerase that can only move in one direction. Second, the strand complementary to a gene's transcription start site is that sequence's complement and therefore not a start site itself. Hope that clears it up. :)


speciation in a single population Most examples of speciation describe a population splitting (via various mechanisms) into two or more populations that eventually become separate species from one another.  However, what if the population never splits? In other words, at some point in the evolution of a single species, an individual member would become (theoretically) unable to reproduce with its own ancestors--thereby becoming a distinct new species.  How can we say that this has happened, given the impossibility of the example?

Allopatric speciation

  Allopatric speciation [..], also referred to as geographic speciation, vicariant speciation, or its earlier name, the dumbbell model, is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with gene flow.

Sympatric speciation

  Sympatric speciation is the process through which new species evolve from a single ancestral species while inhabiting the same geographic region. In evolutionary biology and biogeography, sympatric and sympatry are terms referring to organisms whose ranges overlap or are even identical, so that they occur together at least in some places.

Yes, sympatric speciation appears to be a thing but estimates of how common that is avery hard to come by.

Now, what you describe is not so much sympatric speciation as you refer to a case of reproductive isolation between extant individuals and their ancestors. I am not sure that was really what you had in mind because otherwise you would have not put it in opposition to allopatric speciation but it is what you seem to phrase. Of course, such type of "temporal reproductive isolation" is obviously a thing.


Where can I find a list of diseases and their incidence? Say I am studying a particular disease and I know that its incidence is 0.8 per 100000 children below the age of 18, how would I find the incidence of a whole bunch of other pediatric diseases (or even not just limited to pediatrics)?

Essentially I want to find diseases that would be familiar to a medical audience and provide an example of a disease with an incidence of about 0.8 per 100000, another one that is one tenth the incidence and another one that is ten times the incidence.

About diseases in general, that would concern the health dept. of the respective country government, and the govt. is the most probable source for such numbers.

However, orpha.net has two reports with numbers concerning hereditary diseases, have a look at http://www.orpha.net/consor/cgi-bin/Education_Home.php?lng=EN#REPORT_RARE_DISEASES


Can someone help me to identify what kind of pear is this? I went to my local groceries supermarket (in Lima, Peru) and found this cheerful looking pear named locally as "pera canela". But I found it weird as the only variety which I'm aware of is Packham's pears. I tried to do some research on different cultivars and species known of pears. So far the only ones which I found were in this wikipedia's entry but it didn't help me much.

Below is a set of pictures I took of the pear referred to as "pera canela"

Figure 1. Picture of packed Pera canela, the printed label shows its local name.

Figure 2. Picture of Pera canela's as they are on a basket in groceries stand. Seen in the background.

Figure 3. Picture of Pera canela seen closer for identification.

I've tasted it and it is a little bit more sweeter than the Packham's variety, on the juicier factor I would say that it is pretty much the same as Packham's

So far by comparing it with different entries on Wikipedia. I'm not very sure if it's a local name given to either Abate fetel or perhaps to Bosc
 varieties, or could it be a D'Anjou?

Since I'm not good at identifying plants, can somebody help me identify which kind of pear it is? It would also greatly help me if the answer could include its scientific name so I could do more research into it.

Plu Code 4413 is a bosc pear (a cultivar of Pyrus communis).

From the PLU search tool available via the International Federation for Produce Standards

FYI: take a close look at the pear you're holding in your picture:

Pera canela, meaning "cinnamon pear" in English, is in reference to its color. From Wikipedia:

  Famous for its warm cinnamon color


Am I entitled to the latlong coordinates of all specimens used in a species revision paper? If someone publishes a species revision with distribution maps but without publishing all the data used in the paper itself - or in an attached or linked-to  file - are the authors nevertheless required to make all the data necessary to the paper publicly available on request?

I'm assuming they are as this makes sense from an accountability & replicability perspective (and nonsense of the idea of "publication" otherwise?) - but it's not clear to me from searching online.

Thank you!

No - you're not entitled to anything. Authors may refuse to share because they want to control future publications arising from their data, either simply to inflate their own publication record or to prevent certain types of anlaysis of their data (see the 'data parasites' fiasco last year for an example of attitudes towards data sharing in some parts of the medical community - this, this, and others).

Alternatively they may simply no longer have the data. Nowadays this is less common, but if you contact an author about a publication from the 1960s it's pretty unlikely that any unpublished data is still in usable form.

Finally, certain aspects of data may not even have been recorded. Before GPS was widely used, accurate lat-longs of collection sites are unlikely to have been measured. As @Kara notes in the comments, it is not uncommon for the collection sites of older samples to be recorded at the country level.

This is why journals are increasingly adopting data-sharing policies (see BES, for example)

However, many authors are happy to share their data, and you lose nothing by asking. Good luck!


Why do marine animals have fins? Why do Marine animals have fins.

It is more efficient to use fins than feet, hooves, or other similar body parts. It is the same reason that you can swim faster while wearing flippers. Having a larger surface area allows animals to push against more water, so that they have more force when swimming. Here is a picture of the bones in a dolphin fin. They are extremely similar to the bones in a hand, because dolphins evolved from land animals that had individual fingers.

Amphibians like frogs and salamanders have webbed feet, which is a "compromise" between feet and fins. These feet allow them to push against water with more power, since they have webbing instead is separate fingers. It also allows them to grip the ground on land, since their fingers can move independently of each other.


Solvent Accessibility, the 20% cut-off method I'm reading the papers linked below and all three of them mention a 20% cut-off for buried/exposed residues, by calculating a relative solvent accessibility (RSA) value.

I understand how the RSA is calculated, by dividing the calculated solvent accessibility against its total solvent accessibility values from paper 4 table 2.

RSA = calculated/total

e.g. if arginine is calculated to have a solvent accessibility of 55.43 and its total solvent accessibility is 241 then the RSA = 55.43/241 = 23%, so this arginine is considered exposed (see statement 1 below).

What leaves me confused is the definition or lack of the 20% method for defining an exposed or buried residue.

I am assuming it means one of the following:

If an amino acids RSA is below 20% it is buried and above 20% it is exposed. So for an amino acid with an RSA of 21% is considered exposed, this value seems a little low for me. I think statement 2 would make for sense.
If an amino acids RSA is below 20% it is buried and above 80% it is exposed.

Which statement if any is correct?

Paper 1 - see methods section first paragraph

Paper 2 - see figure 5 and table 3

Paper 3 - see abstract and dataset

Paper 4 - see table 2 for total values

Its 1.  Below cutoff, buried, above cutoff accessible.

Paper 1: "A cutoff of 20% was used to define the two states, buried or exposed. With this definition, the dataset was, roughly, evenly split between the two states."

Only two states are possible: solvent accessible and buried.

Paper 2: "A given residue is defined as exposed (e) if its RSA is larger than the cutoff
value, and otherwise it is defined as buried (b)."

Abstract for Paper 3: a cutoff of 20% for two-state definition of solvent accessibility.

If it were def #2 it would be a three state definition.

Paper 4: "On average, 15% of residues in small proteins and 32% in larger ones may be classed as “buried residues”, having less than 5% of their surface accessible to the solvent..."

This paper, by the dean of structural analysis Cyrus Chothia, uses a 5% cutoff, not 20%...

The abstract goes on to say... "The accessibilities of most other residues are evenly distributed in the range 5 to 50%."

This passage hints that SA doesn't even go up to 80%.  Just considering that you often won't get more than say 60% with this calculation.  I'm just guessing; but the thought being that unless you are at a terminus of the protein, which is often disordered and doesn't show up in a crystal structure, you will have two adjoining amino acids for each residue - just the solvent accesible area taken up by the contact with neighbors could easily be 20% of total.


What is this fruit found in a market in Uyuni, Bolivia at the end of December 2019? (orange skin, 4cm, white flesh) What is this fruit found in a market in Uyuni, Bolivia at the end of December 2019?

Fruit diameter: ~4 cm. Seed: large, spherical, black. Flesh: white. Taste: sweet but not as sweet as a lychee.

I found the name: it appears to be Garcinia humilis, known commonly as achachairú or achach:

  Garcinia humilis, known commonly as achachairú or achacha, is a small, prolifically-fruiting tree related to the mangosteen. It grows in the southern part of the Amazon basin in the central area of Bolivia, but has recently been planted on a commercial scale in Burdekin, Australia.

That matches the area, appearance and season.


Luciferase promoter vector over p-AcGFP1-C1 vector AcGFP1 vector can emit light by itself, whereas in case of Luc vector a substrate is needed for the reaction. Nevertheless, Luc is said to be more specific or better than AcGFP1. Why is this so called? What are the advantages of Luc vectors over AcGFP1?

You are confusing luminescence and fluorescence. GFP does not emit light. The abbreviation stands for Green Fluorescent Protein. You need to shine a blue light source at it and it will fluoresce green. The problem is that many organisms have background fluorescence, a cell without any GFP can often have a little bit of fluorescence by itself or contain pigments that mask the signal.

Luciferase assays depend on a chemical reaction which oxidises a molecule (luciferin in the case of firefly luciferase) and photons are emitted.  This is much more sensitive than fluorescence but is also a lot more expensive and usually (but not always) requires cell lysis. It is very rare for a cell to emit light by itself so the background will be a lot lower allowing you to see smaller difference.

There are many reasons to choose one over the other in an assay, if you share a bit more on how you intend to use the reporter you can get a more detailed answer.


Function of NaCl in yeast shuttle prep of plasmids What is the role of NaCl in plasmid isolation from yeast cells using plasmid rescue solution? If the basic theory behind the method is alkaline lysis, then we is NaCl used and not NaOH?

High salt concentrations will cause the proteins and lipids to precipitate out, as in salting out. Free Na+ ions may also bind the negatively charged DNA backbone and give the molecules a neutral net charge, allowing them to concentrate as well.


Why isn't photosynthesis catabolic reaction? Here is the chemical equation of photosynthesis

$$CO_2 + H_{2}O \longrightarrow C_{6}H_{12}O_{6} + O_2 $$

We see that the water is in reactant side of the equation. By the way, It ought to be catabolic reaction. However, It seems anabolic reaction on my textbook.

What should we think for this reaction?
How do we get If energy turned out in product side of the equation?
Why isn't photosynthesis catabolic reaction?

Catabolic reactions are those that make larger/more complex molecules into those that are smaller/less complex, releasing energy.

Anabolic reactions are those that makes smaller/less complex molecules into those that are larger/more complex, costing energy.

Photosynthesis takes two of the least complex molecules from the perspective of biology, carbon dioxide and water, and forms glucose which is high-energy and complex - this is clearly an anabolic reaction.

The only way I can interpret your question is that you were misunderstanding the definitions of catabolic and anabolic.


Difficulty in developing certain vaccines I have a college level background in Biology, say at the level of Campbell. I am very curious to know why it's extremely difficult to develop vaccines for certain diseases. Two cases which I am really interested in are Malaria and AIDS. It would be great if someone can give a brief sketch of the major issues being faced without getting into extreme technicalities. Thanks in advance.

Not an easy question, especially since the reasons for both pathogens are different.

For HIV the problems are manyfold:

Insufficient knowledge about required immunity

Its not known, which parameters are really important to raise an adequate immunity.

Variation in HIV strains

HIV has a very high mutation rate, which results in many different subtypes. This makes the virus extremely successful, but also causes problems for making vaccines. We have a similiar problem with vaccines for the flu, but there the number of subtypes is known and not very high. Still we need a new vaccine for each season based on the current viruses. For HIV there are no knwon proteins against which immunity can directed like in the case of the flu.
HIV also recombines very fast, so new variants can come up pretty fast.

HIV targets the immune system

The HI virus targets cells of the human immune system (namely CD4 T-cells) which are important for developing a proper response to a vaccination. These cells need to be stimulated, but on the other hand are destroyed and specially targeted by the virus.

Lack of an effective animal model

To develop and test good vaccines, scientists need good animal models to test the pathogen and see the effect of a treatment.
Chimpanzees show some response to HIV infections, but they are expensive to keep as laboratory animals and also rare to get. The problem is, that HIV is pretty good adapted to its human host.

Human subjects trials

This is more an ethic problem, but still needs to be adressed. To test the efficiency of new drugs, double-blinded placebo controlled test are done. Afterwards you can compare the placebo group to the treatment group and analyze the outcome. How do you do this with a deadly disease?
More information can be found on this webpage from the NIH.

For malaria some of the problems are similiar, others are different. he greatest problem was for years, that not enough money was available for research, which has been overcome only quite recently:

Plasmodium goes through different stages

The parasite causing malaria goes through three different stages in its development in the human body. With each step it hides again from the immune system. The different stages are also present in different cell types, see this image from JCI ("Advances and challenges in malaria vaccine development"):

antigen

Its not clear, against which antigens such a vaccine shoud be directed. This is due to the problem with the different stages and hasn't been found yet.

different pathogens

There are four forms of plasmodium which definitely cause malaria - : Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale and Plasmodium malariae. Newer results suggest, that Plasmodium knowlesi is also a pathogen for humans.

lack of animal models

More information can be found here.


Understanding what passes through and doesn't pass through the plasma membrane I have difficulty in understanding the reason why certain molecules can pass through phospholipid bilayers.

Firstly, I understand that the outer layer of the lipid bilayer is hydrophilic - my understanding is that they "like water" and can interact better with water.

Bilayers can absorb hydrophobic substance like N₂ and O₂.

Does this mean - because the hydrophilic surface are capable of hydrogen bonding - that's why they are able to absorb hydrophobic substances like F , O and N ?

They can absorb non-polar molecules.
They can absorb small uncharged molecules like H₂O and CO₂.

I'm not sure of the reasons behind 2 and 3 ...

And of course , vice versa ... (what can't pass through the lipid bilayer easily).

Any help would be appreciated!

Great questions! Your 3 questions can be answered in 2 parts:

1. How do small, uncharged gasses (ie: O₂, N₂, CO₂) diffuse through lipid bilayers?

First it's important to clear up some terminology: Absorbing a compound isn't the same as being permeable to that compound. If you say that a compound is absorbed (or partitions) into a bilayer, you're assuming that the absorption of the given compound by the bilayer increases the entropy of the system (and is thus energetically favorable). For example, lipophilic compounds partition into lipid bilayers because of the hydrophobic effect; by partitioning into the bilayer they break a number of hydrogen bonds and thus increase the disorder of the system.

Small, dissolved gasses like O₂, N₂, and CO₂ are not absorbed into lipid bilayers, they simply diffuse through passively because of their small size and because they are non-polar.

Water is also able to passively diffuse through a lipid bilayer even though it is polar. We might think it should be fairly rare for a polar water molecule to pass through the hydrophobic center of a lipid bilayer, but typically living cells are found in aqueous environments, where concentrations of water outside the cell are extremely high, so this does occur at biologically relevant rates. In fact, the passive diffusion of water in and out of cells is so important that many cells have developed special transmembrane proteins to facilitate the passage of water in and out of cells (most notably aquaporins and pressure-gated channels).

2. How do non-polar molecules pass through lipid bilayers?

This is answered in the related question posted in the comments section of your question. Briefly, it has to do with the same electrostatic problem I mentioned above: Though there is an energetic cost for non-polar compounds to pass through the hydropilic layer of a lipid membrane, in most cases the partitioning of the compound into the membrane still raises the overall entropy of the system (due to disruption of the hydrophobic effect), making it an energetically favorable process.

It should be noted that for the most part, polar compounds do not spontaneously cross cell membranes because of the hydrophobic region of the lipid bilayer. When passage of these compounds into or out of the cell is required for life, cells typically produce transmembrane proteins which can act as either active or passive transporters to allow these compounds through.


Wim Hof Method claims Alkaline Blood is Good. Contradictions? Counterproof? The Wim Hof Method claims, that it is beneficial to have alkaline blood.

On the other site there is the medical claim that if the pH-value is not within the
range of 7.36 – 7.42, enzyms are not functioning properly and their 3D structure could be broken (denaturation). The correct pH-value is also invaluable for exchange of gases/O2/CO2, proper function of muscle contraction and
nerve conductivity.

So: What is this all about and how can this method be so good? After all, they also have conducted medical studies, so there must be some truth in it?! Thanks!

The Wim Hof method unfolds its health effects by hormetic stressors, respiratory alkalosis is one of them (a minor one). The WHM does not follow the pH theory, even though Wim himself gave ambiguous statements in older interviews about this. There are many people who misinterpret the WHM breath work as plain hyperventilation, which is very wrong. It involves a hyperventilation phase in preparation of a hypoventilation phase. This is similar to apnea protocols. The hyperventilation phase itself can mediate minor health effects. As it is not a chronic practice but relates to a few minutes per day, the stress of respiratory alkalosis is very likely within the hormetic range, hence beneficial. The WHM does NOT advocate continuous hyperventilation, which is known to be linked to chronic disease (exceeding the hormetic window).

The clinical trials of the WHM are peer reviewed and well conducted. However, people tend to mix Wim's interviews with the clinical evidence, which is obviously bad. The major paper (group study with control group) is this one: https://www.pnas.org/content/111/20/7379.full.pdf

It clearly shows the anti-inflammatory effects and increased leukocytosis of the breath work (intermittent hypoxia) and also shows that blood pH correlates to the respiratory rate, more precisely blood CO2 levels as expected. Those are normal blood gas dynamics, nothing woo woo pH stuff and no serious scientist would attribute the health effects of the method to the temporary blood pH fluctuations seen from a short hyperventilation phase, especially not when far more dominant and better documented effects on hormonal adaptations can be discussed instead. Some practitioners get quite enthusiastic about urine pH measurements, which are VERY high after the breath work, however all this indicates is normal kidney function in response to temporary respiratory alkalosis, nothing fancy at all. The body increases bicarbonate outlet via the kidneys (renal compensation) when blood CO2 gets too low (hyperventilation) to maintain blood pH homeostasis. the pH strips measure this bicarbonate. Another misconception is that the reading would correlate to progress or health, while it actually just correlates with hyperventilation intensity/duration. It is quite annoying how many misconceptions about simple physiological details float around the web, primarily due to the success of the pseudoscientific pH theory and alkaline diet. I guess some people just got rich with that crap...

Understanding the WHM means understanding hormesis and the stress response in the first place. The whole idea is comparable to physical exercise: stress the body enough to become stronger but not so much to take damage.


Was the mitochondrion or chloroplast first? I still don't  know if the mitochondrion or chloroplast was first? I've looked for it on the internet and in various books but haven't found anything. Does anyone have the answer and a theory which backs up this answer?

Mitochondria evolved before chloroplasts.

We know this because Mitochondria form a monophyletic group: e.g. all life with mitochondria traces back to a single common ancestor (source). Since the group with chloroplasts groups within this clade, it must be the case that either (a) chloroplasts were obtained by an organism that already had mitochondria or (b) chloroplasts were independently lost by multiple lineages within the Eukaryotic clade and then many of these lineages re-acquired chloroplasts by secondary endosymbiosis. Since (a) is a (much) more parsimonious explanation it is the one it makes sense to accept.


Do non-migratory canada geese still exhibit migration behaviors? I have noticed that many of the geese in my region (NE US) remain overwinter. I also see many of what I guess (but am not sure) may be the same geese flying in migration patterns. One thing that makes me think that non migrating geese do this, is that I observe group formations flying in all directions, not just southwards in the fall.

Does anyone know whether the resident geese still like to fly in migration patterns, or is it always the migrating geese that you see doing this?

The answer is yes, also sedentary geese do use migration patterns (V-formations). When they move from roosting place to feeding areas (or vice versa) geese always tend to fly in formations. I speak for personal experience of resident and wintering birds in Europe and America.

They do so because they save energy as explained here: http://jeb.biologists.org/content/128/1/445.short and here: http://www.nature.com/nature/journal/v413/n6857/full/413697a0.html

The second study also show how not all the positions in the formation are the same regarding energy expenditure. The one closer to the front of the V shape need to flap the wing more often.

Have fun


How big is a baby's stomach? There is a lot of contradictory information on baby feeding volumes on the internet. A common claim is that a baby's stomach is the size of a hazelnut or small marble, with a volume of 5-7 ml. But this seems confusing on two counts -

Breast milk contains approximately 0.7 cal per ml, so feeding 6 ml eight times per day would only provide the baby with 33 calories, which doesn't seem enough.
A typical marble is 1/2 inch (1.25 cm) in diameter, which means it has a volume of about 1 ml, not 5-7 ml as claimed.

Are there any authoritative sources on the size of a baby's stomach?

The first 30 days involve rapid growth, but generally, fall within a standard proximal range of 5 - 7mL on day one. By day 3 the stomach has expanded vastly to nearly 23 - 27 mL. From this point on, growth and size to age ratio will vary a bit.

https://themomivist.com/2016/10/10/the-newborn-stomach-size-myth-it-is-not-5-7ml/

Here's a link to an article that has some efficacy. Many hospitals and physicians use different techniques and believe differently on this particular subject. Considering the laws surrounding experimentation on fetus and children, the "Size" of the stomach debate only has efficacy if we were able to case study THOUSANDS of infant stomachs which isn't likely to happen anytime soon. I hope the link helps and maybe points you in the right direction. There really is no 100% correct way to answer this as the studies surrounding it just don't have any weight to them.


Organ cloning - possible to make a non-antigenic organ? From a J. Neil Schulman article on Organ Cloning:

  Cannibalizing organs from other people also entails the risk of
  rejection because of incompatibilities, not only for tissue-typing but
  also for gross anatomical mismatches. Cloning organs [...] has the
  potential of taking a human being's own genetic material and growing
  perfect replacement organs which are fully compatible with their
  genetic makeup.

The reason for using a person's own DNA, is obviously to avoid an allergic reaction to the antigen markers on a strange organ. But in the blood typing system, there exist types which don't have any trouble-making antigens (such as type O-negative, called a "Universal Donor").

Would it be possible to grow an analogous "universal" internal organ, which didn't have any antigens indicating it was a foreign body? (By editing a DNA sample to remove certain expressed proteins, then growing it into an organ.)

I realize this is technically a science-fiction question :) But - A: it may not be in the near future, and B: I can rephrase it to remove the SF component:

In the blood-typing system, the AB antigens don't appear necessary for proper functioning of red blood cells - are the antigens on a person's own cells, actually needed for any essential functions, or could they be removed, without affecting that person's health?

I'll contradict the answer posted here (ages ago) and say no, it isn't possible. Growing an organ wthout MHC proteins might be achievable, but it would be rejected for not having MHC1. NK cells instruct all cells without MHC1 to perform apoptosis. In this case, MHC1 antigens are required on cells for proper self-identification.

Keeping MHC1-less cells alive could be achieved by

equipping them with whatever is keeping erythrocytes and thrombocytes (also lacking MHC1) from being destroyed on sight. (A good idea, but see next paragraph)
disabling their apoptosis mechanism (Cells with disabled apoptosis mechanisms are commonly referred to as cancer, so we might want to not do this.)

MHC1 also has a function; it presents "peptide shreddings" from proteosomes to T cells; this way T cells can check if the cell contains internal foreign proteins (sign of a virus infection or cancerous transformation). Thus, removing MHC from the cells would make them very liable to become nearly unstoppable virus factories or tumor cells.

(On a side note, while everyone technically can receive 0 Rh negative blood, group-identical blood is used always, except in rare emergency cases. A and B antigens here, as far as I know, do not have function.)


Why do the two sexes have different reproductive costs and capabilities? Is there an evolutionary explanation that shows why the reproductive costs are mostly on the female sex?
And therefore, why do males can potentially have more offspring?
Does that happen to create more competition in sexual selection?

I may have misunderstood your question, but there is no theory why usually reproductive costs are on the female, as this is a fact. Females have usually larger (and fewer) reproductive cells (gametes), they frequently have to carry the embryo until birth, and sometimes they have to attend to the offspring during the first stages of their lives. To put it very simple, females are stuck with their offspring from the moment of conception until they are born - sometimes even longer - while males generally can mate with many females in a short period of time, potentially having much more offspring.
A consequence of this is that, usually, females are choosy (they want good mates), whereas males just try to mate as much as possible. Female choosiness generates sexual competition, as females prefer to mate with males having certain characteristics that hint to a superior genotypes/phenotype that may be passed to their prole (e.g. beautiful plumage, social status, size of the wallet). Sometimes the costs of attending offspring after birth are higher than the costs associated with reproduction alone. In some of these cases, we may observe unusual behaviors, e.g. male-only parental care and choosy males.
This is a very broad and complex topic and a short answer here cannot cover all of it. John Maynard Smith developed the game theory approach most commonly used to investigate the consequences of different pay-offs for the two sexes and to explore how these can influence the behavior of the parents. Moreover, this topic is also covered in many behavioral biology textbooks. I have had very positive experiences with Krebs & Davis Behavioural Ecology (ISBN-13: 978-0865427310), which I would recommend.
Hope to have clarified some of your doubts.
Cheers,
Emilio


What is this little white creature? Please identify this little and soft white creature. Since childhood I am seeing this things flying in my surroundings and nowadays they are seen occasionally.

It is, as stated by @rg255 a seed (or actually a fruit, see below). The seed itself is the small brownish thing. The white hairs are attached to make the seed fly with the wind. Looking at the seed and the hairs, I think the seed belongs to the daisy and dandelion familie asteracae/compositae. Altough there are other possibilities, see comments.

EDIT:
@AlwaysConfused is right if he states that in case of daisy family, it should be called a fruit, that containes one single seed. To be more precise, it is an Achene/Cypsula. In many species, what is often referred to as the "seed" is actually a fruit containing the seed. The seed-like appearance is owed to the hardening of the wall of the seed-vessel, which encloses the solitary seed so closely as to seem like an outer coat. Info derived from here on fruits and seeds and more specifically on Achenes/Cypsela here


Breakdown of energy expenditure at the level of a single cell The metabolic rate measures how much energy an organism expends over a unit of time. Its breakdown for the human body in terms of its functions is well documented : so much for the heart, for the brain, etc.

In West et al, 2002 I have found an estimate for the metabolic rate of a single cell. But how does this breakdown in terms of elementary functions in the cell?

E.g., how much of the energy made available from nutrients is used in the process of replicating genome, of expressing proteins, of trafficking...?

Following Jeremy Kemball's link suggestions, I find in this paper the fraction of ATP consumption for the following processes:

Protein synthesis    0.34
Na+/K+ ATPase        0.16
Ca2+ ATPase          0.17
RNA/DNA synthesis    0.25
Unidentified         0.09

(which adds up to 1.01 rather than 1 for spurious reasons). Their measurement is indirect, based on $O_2$ consumption for an assumed steady-state regeneration of ATP. I wonder how GTP-based processes are accounted for? Or are they negligible compared to ATP ones?

This is for a specific cell type, rat thymocyte, is there a reason to expect that this will be hugely different for say a fibroblast? Also, they stimulate their thymocyte with concanavalin A. I understood they are not getting RNA/DNA consumption signal without Con-A, but didn't get why it would be so.

Finally, what would be in the remaining 9% ? One candidate for ATP consumption suggested by Jeremy Kemball is actin turnover, I guess it fits only in the "unidentified" line. Tubulin turnover is a GTP process, not sure about intermediate filaments (do they turnover?). All ATP-molecular motors (myosin, kinesin, dynein at least?) have to be there too.  What else?

I am particularly interested in the total amount of ATP energy that goes to myosin.

I was musing on this and did some strange googling, and have some ballpark figures  for a bunch of different organisms. It's far from a complete answer but it's at least a start, and all this won't fit in a comment.

DNA replication, I assumed, was a huge metabolic drain on the cell. Turns out that is far from the case. Many helicases are passive, requiring no ATP, and the amount of ATP-equivalent triphosphates to synthesize the entire genome is pretty small compared to the amount that gets used and recycled every day.

According to these guys humans go through their bodyweight in ATP every day, about 50% of which is actin turnover, and 30% is synthesis (60% or more in rapid bacteria). Proteins cost about 4-5 ATP per AA to break down and rebuild.

You're not going to get a really good general breakdown, I don't think, but in crop plants or E. coli there are numbers for this, sort of. A lot of them are based on indirect measurements of protein uptake/turnover and ATP cost per AA or BP. They're fascinating but insane and often contradictory.


What is the "leaky valve" between the esophagus and stomach? When someone talks about there being a "leaky valve" between the esophagus and the stomach, what is the exact biological structure they are talking about?

This would be a structure that, when malfunctioning, causes stomach acid to leak into the esophagus.

The structure is called the lower esophageal sphincter:

Basically, its function is to prevent the contents of the stomach, including stomach acid, from "backwashing" into the esophagus. The stomach is protected from acid by a protective layer of mucus, while the esophagus is not, so any number of medical issues which cause problems with this sphincter may lead to erosion in the esophagus, which is quite painful and can lead to serious long-term consequences if not addressed.


Are drones from one honey bee queen all clones? The Honey Bee queen lays eggs that develop into worker bees (female) if she fertilizes the egg.  If she does not fertilize the egg, it will develop into a drone (male).

The drone only has the queen's DNA so are all drones exact copies of each other, ie clones, or is there some other mechanism that will make each brother slightly different?

The queen is diploid; the drones are haploid. Meaning the queen has two copies of each chromosome, and the drones have only one. So for each gene, the queen has two copies and passes one of those copies on to the drone.

This means the drones are different for exactly the same reason female bee siblings, or human siblings, are different: because every parent has two copies of a gene, that are often different, and passes only one of those to their offspring.

If the queen were homozygous for every allele, i.e. the two copies of all her genes were identical, then the drones would indeed be genetically identical. But this is true as well of the children of two completely homozygous parents.

See this page on inbred laboratory strains of animals (animals which are inbred to the point they and their offspring are genetically identical to each other):
http://isogenic.info/html/inbreeding___it_s_effects.html

  F1 hybrids, i.e.  the first-generation cross between two inbred strains, are isogenic but not homozygous.

In other words, if you have two parents who are genetically different, but have two identical copies for all of their chromosomes, their children will be isogenic (have exactly the same genes); they all have two copies of their genes, got one copy from their father and one from their mother, and those two copies might be different from each other (their mother and father have different alleles), but all the children got those same two copies because they're the only copies their mother and father have.


Does this leaf belong to carissa macrocarpa? I have a picture of a leaf and I am trying to find it's scientific name. The closer I got is Carissa Macrocarpa based on thorns alignment. If I am wrong, I need help in identifying correct species.. Thank you very much in advance!

Edit: Adding some more images

This plant seems to be Carissa carandas. With the thorns placements besides leaves, I was sure that this plant belonged to genus Carissa. Taking advice from Bryan Hanson, I searched for the plants in the same genus in my locality(Hyderabad, India). The white flowers and their rosy stalk made it easier for me to search. I found out that this is a common plant in country side and is used in many dishes. Thanks Bryan for pointing me in the correct direction.


What histological stain can I use for beta-keratin? I'm trying to find a histochemical stain for beta-keratin, the type found in Reptilia which is organized in beta-sheets. It's different than alpha-keratin which is found in mammalian skin, hair, nails, etc., and is formed of alpha-helices.

Simple searches have produced results specific to mammals and alpha-keratin. Are there any good stains for beta-keratin?

Not sure if this is what you are looking for, but I did some searching around for histochemicals and reptilia.  I did come across a paper by L Alibardi, Dipartimento di Biologia evoluzionistica e sperimentale, University of Bologna, Bologna, Italy.  Now, that exact application doesn't seem to answer your question, it did open up a web page that contained numerous papers on reptilia and their beta-keratin structure and investigations into that (citations of the original paper, as well as papers by the same author).  I didn't see any that specifically spoke to the exact stain used, but then this is a little outside my area of expertise.  Perhaps this link will give you an avenue to pursue?

Wish I could help more.


Examples of seeking behavior by brainless animals Are there any examples of brainless animals (e.g. jellyfish) exhibiting seeking behavior, such as following smell or light gradients towards food, or following hormones towards mates?

Yes, there are plenty of examples! We refer to this seeking behaviour as taxis.

Taxis

There are many types of taxis such as chemotaxis (attracted to chemical stimulus) or phototaxis (attracted to light). A complete list of taxis can be found on wikipedia > taxis.

For the purpose of this answer I will restrict to chemotaxis only

  Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.

Chemotaxis in Bacteria

Chemotaxis is very common in bacteria such as E. coli for example (Macnab and Koshland 1972, Wadhams and Armitag 2004).

Chemotaxis in Plants

Chemotaxis is also observed in plants such as rhibozium spp (Currier and Strobel 1976) for example

Chemotaxis in eukaryotes

Chemotaxis is also found in eukaryotes such as in Amoeba or Tetrahymena (Köhidai 1999,Bagorda and Parent 2008) for examples.

Chemotaxis in animals that have "primitive" brains

Nematodes (Ward 1973) and plathelminthes (Bone 2012) for example show chemotaxis.

Chemotaxis in "brainless" animals

Evidence of chemotaxis also come from Echinodermata (sea stars, sea urchins and others) (Miller 1985).

Echinodermata have quite definitely no brain!


Can Rubella virus pass into brain stem? B19 virus (about 20 nm) can; which I think is partially because of its small size; not sure of genomics has something to do with the passing. Rubella's (also called German measles) size is then again minimum 45 nm.
So I started to think if this virus can pass into the brain stem.

Can Rubella pass into the brain stem?

Some studies are made about Rubella associated hemolysis.
I think it is not related with this question at all.
Rubella is diffused along carbon dioxide from capillaries into the brain stem, this is my hypothesis.

It obviously can do that, causing a rubella encephalitis. A specialized form seems to be the "Progressive rubella panencephalitis", which is very rare with only 20 cases described since its first description in 1974.

About rubella encephalitis more papers are available, see these for a start:

Neurological aspects of rubella virus infection.
Mumps encephalitis: return with a vengeance.
Neurological Aspects of Rubella Virus Infection


Is it possible to guide animals to a new breeding ground? (This is a question for a book I'm working on.)

One of the threats to some animal species is the disappearance of breeding grounds (because of the spreading human population, or for example because of ship routes).

Hypothetically: would it be possible to encourage a species to breed on another place? Has that ever been tried? What do animals do naturally - do they seek another location, or rather keep trying?

The problem that you mention deals primarily with habitat fragmentation, which has a great impact on species conservation. A fragmented habitat will impair migration and can result in inbreeding depression. This has been dealt with wildlife crossing in various sites in the world.


How does a jumping spider manage to "jump" on the ceiling? I just witnessed a small jumping spider jump on some kind of louse or bed bug on the ceiling. How does it do that without falling? I have yet to find a high-speed-camera video of a jumping spider jumping on a ceiling.

My hypothesis is that the spider would spit silk and anchor it on the ceiling, then jump, and allow itself to be swung by the silk onto the prey. But I don't have a high speed camera to prove that.

EDIT:
I now have some evidence that supports my hypothesis: I just saw a jumping spider attempt to jump on a prey and failing to land properly. It didn't fall directly to the floor. Instead, it dangled from its own silk, at about 2 cm from the ceiling, then climbed right back up the thread of silk, onto the ceiling.

You are right - most jumping spiders have draglines they secure to the surface before they jump.  They can't defy gravity, but they can recover from a miss if they do this.

  Disturb a jumping spider on a wall, and watch it seemingly defy gravity: it will jump horizontally out into the air, then return to the wall.  This seems fantastic until you spot the major ampullate dragline.  It essentially becomes the bob at the end of a pendulum string.

the book goes on to explain that the dragline is used as an airbrake and a spring to help the spider control the jump, which might make it seem to do unnatural things when jumping from a ceiling.  You might want to get a video of this if you can.

Some of the references in another book here, point to other uses of draglines - the spiders can tell each other's species by them, attract a mate.


Does transplanted heart have full sympaticus without medication? I am reading this and this where I am considering this sentence

  [N]o baseline parasympathetic innervation [in transplanted heart].

Does this sentence imply that the heart work then in full sympaticus all the time?
Probably, through altered systems, but still.
At least the regulation of blood pressure strongly supports this, here for the generic medication plan.

Does transplanted heart have full sympaticus without medication?

Notification of terminology. I tend to use overloading in writing.
For instance, I can say that there is sympathetic and parasympathetic supply to the heart i.e. innervations of S and PS through endocrine system to the heart.

I am not yet completely sure how the recipient's body can target the alpha and beta receptors of donors in heart. Are there any variations of these receptors? If yes, then the effect of sympathetic stimulation would also differ from the original stimulation.
So full sympaticus (or original) may not be present.
The new stimulation may lead to greater or smaller activation of sympaticus.

The parasympathetic supply to the heart is by nerves and that is truncated during surgery as pointed out.

The sympathetic supply to the heart is by two means:

Through sympathetic nerves from the sympathetic trunk
From the adrenal medulla which secretes both adrenaline and nor-adrenaline directly into the blood stream

The heart contains the beta receptors for the sympathetic system, especially the ventricles and nodes (SA) and conducting fibers. These receptors respond to the presence of adrenaline and nor-adrenaline in blood. Thus the sympathetic response is preserved while the parasympathetic responce is lost.

There is a minimal level of nor-epinephrine in blood at all times which thus influences the heart.

Receptors in Heart:

The heart contains adrenergic (sympathetic) and cholinergic (Parasympathetic) receptors. When the heart is transplanted, the donor heart also contains the same receptors. The only thing missing are the nerves.

The sympathetic system does not suffer as much as the parasympathetic system, because of the adrenal medulla which secretes the nor-epinephrine (same as nor-adrenaline) into the blood, which upon reaching the heart can stimulate the beta receptors on the heart.

There is no organ which releases acetyl-choline into blood, (fortunately, as such a release would be disastrous leading to shock and rigor, possibly death). So the parasympathetic receptors in the heart do not receive any stimuli.

Edit 1:
In response to your edit, yes there are polymorphisms in all receptors. But the structure of adrenaline and nor-adrenaline are pretty much constant. This means that the donor heart will be at a similar level of sympaticus as it was in the donor when (s)he was alive. Although this will not be the same as the recipients pre-surgery sympaticus state of the now removed heart.


Can oxytocin travel from one cell to another via gap junctions? Oxytocin is a 9-residue secreted peptide. As a hormone, can it travel through gap junctions, assuming that it is stored in pre-synaptic neuronal vesicles?

Synaptic vesicles are on the order of tens of nanometers (for example Zhang et al give a mean diameter around 40 nm).
Gap junctions are much smaller, on the order of 1-2 nm. Maeda et al measure one at 1.4 nm.
Peptides the size of oxytocin present in the cytosol could theoretically travel through gap junctions. Vesicle-packaged peptides or molecules of any size cannot.

Maeda, S., Nakagawa, S., Suga, M., Yamashita, E., Oshima, A., Fujiyoshi, Y., & Tsukihara, T. (2009). Structure of the connexin 26 gap junction channel at 3.5 Å resolution. Nature, 458(7238), 597-602.
Zhang, B., Koh, Y. H., Beckstead, R. B., Budnik, V., Ganetzky, B., & Bellen, H. J. (1998). Synaptic vesicle size and number are regulated by a clathrin adaptor protein required for endocytosis. neuron, 21(6), 1465-1475.


Is it possible for a human to wake up in a wrong way? There's an old folk saying that goes like "He got out of bed on a wrong foot" - to indicate that the person's day is going poorly because of the way that person woke up.

Is it is possible for a human to disrupt the awakening process, causing negative cognitive side effects for the rest of the day? If so, how long does it take to restore normal cognition?

There's this related question that I asked - if different parts of a human brain can be asleep independently of each other? This question is a variation on that one, and specifically deals with the process of awakening or activating brain regions in the morning.

I'm aware of the concept of "Sleep inertia". However, it does not seem to be the phenomenon in question, as sleep inertia is frequently mentioned in the context of napping. (where napping over a certain time leads to sleep inertia). Additionally, sleep inertia has been described in terms of decline of motor activity, and not as cognitive side effects lasting for a whole day.

From personal experience, it seems that I'm doing best if I get out of bed immediately following a natural awakening, even if it is rather early, as opposed to snoozing for another 30-40 minutes.

I did a quick search and found some research in this area. Sleep inertia is the technical term for feeling groggy for a while after waking up.

In a review article by Patricia Tassi, Alain Muzet (Sleep inertia. Sleep Medicine Reviews. Volume 4, Issue 4, August 2000, Pages 341–353), they define sleep inertia as

  Sleep inertia is a transitional state of lowered arousal occurring immediately after awakening from sleep and producing a temporary decrement in subsequent performance.

and also says,

  Depending on the studies, it [sleep inertia] can last from 1 min to 4 h. However, in the absence of major sleep deprivation, the duration of sleep inertia rarely exceeds 30 min.

Same article reviews several studies (first report in 1964) on sleep inertia relating to sleep stages:

  Abrupt awakening during a slow wave sleep (SWS) episode produces more sleep inertia than awakening in stage 1 or 2, REM sleep being intermediate.

So yes, sleep stage seems to correlate with "waking up in the wrong way" as @CactusWoman suggested.


How deep in the soil can a seed be placed and still develop into a plant/tree? The selected answer to How does a plant grow before photosynthesis is possible? indicates that a sprout grows beneath the soil using the food stored within the seed.

Does this limited ready food place a restriction upon the depth to which a seed may be placed and still develop into a plant? What depth will be best applicable for a given plant/tree seed? Is there a mathematical relationship known?

The general mathematical relationship requires an allometric equation. There are not as many for seedlings as there are for mature trees (but see the answer by @Richard-smith for a specific example). But lets start with a basic assumption that the emerging seedling will be a very tall cone (tall = high h to r ratio).

The volume of a cone is:

  $V = \frac{1}{3} \pi r^2h$

Then we need to know the density of the seedling to figure out how much carbon a seedling of height h would require. Lets say that the density is 1.5 g/cc (excluding water).

Then, assume that the biomass is 1/2 carbon (a fairly reasonable assumption).

To figure out how tall a seed could grow given carbon reserves, it would be necessary to determine the amount of carbon in storage in the seed. Say there were 5 grams. There will be a carbon cost of reallocating this to growth, say 50%. So, for a seed that has 5g of carbon, its total volume might be calculated as:

 (5g * 50% growth respiration)/(50% C content of biomass) * 1.5 g/cc = 7.5 cc

assuming that the seedling will have a radius of 0.2 cm, the height could be calculated as:

  $h = \frac{V}{(3 \pi * 0.2^2)}
    = \frac{V}{0.38}$
          = 20 cm (for V = 7.5)

Note: this is just a very quick "back of the envelope" calculation with many assumptions. C is 50% of plant biomass is pretty close (the actually number is closer to 48%). The growth respiration cost is a very rough estimate, and will vary with nitrogen content of the tissue, soil temperature, and etc.. The plant will likely need carbon left to build a leaf, and another resource may be limiting.


Why is this oxoglutarate dehydrogenase and not oxoglutarate decarboxylase? I was looking at the oxoglutarate dehydrogenase complex and saw the reaction mechanism for its E1-TPP mechanism, which results in the formation of a stabilized carbanion intermediate.
The mechanism begins with a protonation, but since the "goal" of the enzyme is to form the carbanion intermediate, it seems to me that the decarboxylation is the key part of the reaction. So why is this a dehydrogenase-catalyzed reaction and not a decarboxylase-catalyzed one?

I'm new to citric acid cycle and I'm judging this question based on my previous knowledge of biochemistry and organic chemistry.
I've looked into several protein databases and shockingly it seems oxoglutarate dehydrogenase is the correct name for it.( See :Uniprot , PDB 1 , PDB 2 )
Although the nomenclature of biological enzymes sometimes does not sound right to me , I believe this naming is appropriate for this molecule. First take a look at these definitions:
(Definitions from Oxford Languages / Google)

Dehydrogenase :  an enzyme
that catalyses the removal of hydrogen atoms from a particular
molecule, particularly in the electron transport chain reactions of
cell respiration in conjunction with the coenzymes NAD and FAD.

(Wikipedia)

Dehydrogenase (also called DH or DHase in the literature) is an enzyme
belonging to the group of oxidoreductases that oxidizes a substrate by
reducing an electron acceptor, usually NAD+/NADP+ or a flavin coenzyme
such as FAD or FMN.

(Wikipedia)

Decarboxylation is a chemical reaction that removes a carboxyl group
and releases carbon dioxide (CO2). Usually, decarboxylation refers to
a reaction of carboxylic acids, removing a carbon atom from a carbon
chain

Here is why the usage of "decarboxylase" in the name of the enzyme is incorrect :
Recall amylase (Amylase-Wiki) . That enzyme consumes amylose as substrate and produces maltose out of it. It sounds weird if one calls it "Demaltase" just because it gives out maltose. Instead, in this case , consumption of amylose plays a more important role in digestion.
According to above definitions , the "goal" here is simply the movement of H+ and the electron to FAD (to generate FADH2) and then to NAD+ (To generate NADH), Not the removal of CO2. That is just a by-product resulting from the mechanism. see :Reaction
Here's why the usage of "dehydrogenase" in the name of the enzyme  is correct :
Take a look at this  .
The whole process involves the movement of one proton from thiamindiphosphate and one from CoA-SH and also 2 electrons from two S-H bonds (I've traced the Hydrogens for you. Trace the electrons yourself ! :) )
Recall the concepts of carbonyl functional group from organic chemistry. One way to perform any reactions on carbonyls is to use an acidic catalysis which is most of the times H+ resulted from H2SO4 or HCl.Take a look at this. Also see Morrison-boyd organic chemistry or Vollhardt's This H+ Activates the carbonyl functional group , allowing it to participate in nucleophilic substitution more easily. The addition of H+ to Carbonyl oxygen is reversible and thus it is important to optimize this equilibrium. The indicated enzyme operates on this equilibruim to gain the maximum yeild. Plus it may induce TPP to lose a H+ . These two processes (the removal of H+ from TPP and the addition of H+ to oxogultarate ) can not be done with the help of the enzyme , hence the name Dehydrogenase for the enzyme.


Reassociation of DNA What is the order in which this DNA samples would would reassociate ?

e.coli DNA

plasmid DNA

viral DNA

satellite DNA

DNA-RNA hybrid

This is a homework question and I have not been given any information about the condition in which they are reassociated.

The rate is determined by the size and complexity of the sequence. Short, non-repetitive sequences should re-associate (at a given r.t.p.) faster than longer, repetitive DNA.

I'm guessing that that is what this question is getting at.


How does the synaptic cleft exist? I'm not asking why the synaptic cleft exists, i.e. what function it holds, rather how.
So I know that the neurotransmitter diffuses across it, it is 20-40 nm wide and contains basal lamina (in NMJs at least), but I cannot find any allusion as to what causes the gap; how the two membranes don't just touch, and how so consistent a distance is created across neurons.
Google has so far failed me on this one, though perhaps I am not searching well enough, any help would be greatly appreciated.

There are membrane proteins that act as structural components of the gap (i.e. the synapses aren't just floating there, they are anchored to each other via membrane proteins).

https://en.wikipedia.org/wiki/Neuroligin
https://en.wikipedia.org/wiki/Neurexin

The most common examples are neurexin (expressed on the pre-synaptic terminal) and neuroligin (expressed on the post-synaptic terminal). Not surprisingly, these proteins are involved in synapse formation in the developping brain, as well as the adult brain (in plastic processes where new synapses are formed). To a first approximation, as synapses are growing, their membrane proteins bind their partners and become anchored. This also leads to intracellular signalling and further maturation of the synapse. That's how synapses know where to attach.


Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck? Some people who get directly struck by lightning and some more than once (starts at 00:25) survive while others die instantly or later on due to complications/injuries.

Looking at a wiki page for Lightning injuries

  Lightning injuries are injuries caused by lightning strikes.

  They result from three factors:

  electrical damage.
  intense heat.
  the mechanical energy which these generate.

  While sudden death is common because of the huge voltage of a lightning strike, survivors often fare better than victims of other electrical injuries caused by a more prolonged application of lesser voltage.

Lightning can strike or injure humans in four different ways but I'm going to focus on direct strikes.

  Reported mortality rates range from 10–30 percent, depending on the source of data. Most people who are struck by lightning live to tell the story, but many suffer from long term injury or disability.
  Airforce medicine site

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

To be lethal a lighting strike has to do enough damage to a critical organ that the injury is not survivable.  Since electricity can take highly variable paths through a body, the amount of damage inflicted is also highly variable.

For example, current entering on the head and exiting on the foot stands a good chance of passing through both the brain and heart.  This is likely to be a very severe injury.  Conversely, current entering on the left hand and exiting on the left foot does not cross the body and may leave superficial burns but limited internal injuries.


Anomalous base pairing of nucleotide tautomers What tautomers base pair with what bases?

I know that adenine pairs with thymine and guanine pairs with cytosine normally. My question is what does the imino form of adenine base pair with? Regular cytosine? What does the enol form of guanine base pair with? Regular form of thymine?

I cannot find any books discussing this issue and Google is of no use. However, my professor wants us to know how tautomers base pair.

I tried base pairing cytosine with adenine but does the -NH2 group on cytosine really hydrogen bond with the imino -NH group on the adenine tautomer?

The tautomers are rare but they can form and it is suggested that tautomerization can lead to mutations because of non-cognate base pairing.

Khuu & Ho (2009), have inferred the presence of adenine and thymine tautomers from the crystal structure of an in-vitro assembled holliday junction. They infer that imino-Adenine base pairs with amino-cytosine (normal form) and enol-thymine base pairs with keto-guanine (normal form).

  Reproduced from: Khuu & Ho (2009)

Khuu, P., & Ho, P. S. (2009). A rare nucleotide base tautomer in the structure of an asymmetric DNA junction. Biochemistry, 48(33), 7824-7832.


Do ants within a colony ever fight or come to conflict? I'm investigating how hierarchical groups of a larger organization with a common goal tend to come to conflict with one another over time.  As you decompose a large group (for example a corporation), peer groups may compete in an effort to accomplish short-term goals in an effort to further the corporation as a whole.  For example, two groups of software developers might fight for time on the corporations computer system to finish their immediate deadlines.  Though this typically can be resolved through mediation and compromise, there is a human element where one group might inflate the real need to use such a resource.

I was then wondering if the same situation could ever arise in an ant colony.  Are ants truly purely social and never come to conflict within a colony?  Or can they end up fighting internally if food or space is ever scarce?

There has been several major transitions (John Maynard Smith and Eors Szathmary) and systematically there is opportunity for conflict to arise…. and it does! There is conflict along genes within a chromosome (example the Psr gene of Nasonia vitripennis, see R. Trivers and A. Burt Genes in conflict), along chromosome within an individual and along individual within a colony.

Ants has been much studies (see E.O. Wilson, L. Keller, M. Chapuisat) and it has been found that there are tons of different reproduction system in those species. There are conflict between queens, between workers and between queen and workers to reproduce. In some species, a colony have several queens, in others, there are several queens fighting early in life for the right of being the unique queen. In some species, workers can fight to take over the queen and take her function. In some species, workers reproduce sometimes even if there is a queen. There is conflict over who will survive depending on how much related one is to the other one. For example, there is conflict over sex-ratio, the queen is as much related to her sons than to her daughters but the workers are more related to their sisters than to their brothers (because of haplo-diploidy, see Robert Trivers).

There are various factors limiting the conflicts: high relatedness (Hamilton, Trivers), Cost of a fight, absence of information, power asymmetries. Ants evolved various strategy. There is a "police" who kill worker's spawn. We might as well consider lineage selection that select for cooperative colonies (note that L. Lehmann and L. Keller argue that group selection and kin selection are the same concept!)

I basically repeated some stuff I read (or learned in class) but I am personally not sure that all that makes sense! I don't know if really the frequency of conflicts is not simply related to the mutation-selection balance. Criticisms are welcome!

UPDATE:

In reaction to your comment:

Conflicts always have to do with reproduction or survival in evolutionary biology. One might make three categories of conflict:

1)Those involving the right of reproducing

2)those involving the probability of dying (I prefer not to be a forager because forager have a very high mortality)

3) Those that concern the survival of kin individuals. The "purpose" (if I might use this agency way of speaking) of any one to to increase its inclusive fitness (Hamilton, but don't read Hamilton, there is lots of easy source of information on kin selection). Therefore, one will rather help its brother to survive rather than his cousin as it is more closely related to its brother. Similarly, beccause of the haplo-diploidy nature of sex determination system in hymenoptera, workers are more closely related to other workers than to the males while the queen is as much closely related to her daughters and sons. Therefore, we would expect a conflict over the sex ratio, queen trying to have a sex-ratio of 1:1 while the workers are trying to have a sex-ratio of 75:25 (if there is only one father).

Hope this helps!

If you want more specific information about sex-ratio in ants, kin selection, group selection please ask it in another post. Note that there is already some discussions one these subjects on Biology.SE.


Does bioluminescence occur in humans too? I read that Japanese researchers have developed very sensitive camera that recorded bioluminescence in humans; is it possible and if so what is the mechanism behind it?

From the article you linked:

  virtually all living organisms emit extremely weak light, spontaneously without external photoexcitation. This biophoton emission is categorized in different phenomena of light emission from bioluminescence, and is believed to be a by-product of biochemical reactions in which excited molecules are produced from bioenergetic processes that involves active oxygen species

They reference these two works. The first is a 1988 review from Popp et al. (1988):

Biophoton emission - Experientia 44:543–600. (sorry, I cannot find the link to a full text...)

Fritz-Albert Popp is the biophysicist who first developed the biophoton theory.

The second work they reference is by the same first author:

In vivo imaging of spontaneous ultraweak photon emission from a rat's brain correlated with cerebral energy metabolism and oxidative stress. - Kobayashi M, et al.

Finally, a search in Pubmed reveals various other articles by different authors studying different species.


What is the name of this about 5cm high, grey, Beanie shaped fungus? I found those below some stone stairs in Germany. The grass gives you an impression of the size (I guess the grass is about 5-7cm tall)

I think this is Coprinellus disseminatus, also known as "Fairy Inkcap". Size (they are pretty small) and also the color fits pretty well. See the image from the Wikipedia:

Some more information can be found here.


Flower identification: Moscow, Russia I found this plant near the MSU, Moscow, Russia. Could someone help me to identify it?

It looks very similar to Cephalaria gigantea.


Does amylolysis occur in vegetables if stored below 0⁰ Celsius? Assume that we have a plant, e.g. kale, which is prone to amylolysis if not harvested during a frost period.

If it is harvested and put in a household freezer, such that it is frozen solid slowly enough for cell walls to burst, will the amylolysis stop, or will it still occur? Will it occur if it is kept in a fridge in the 0-4 Celsius range? If it does not occur while the vegetable is frozen, will it start after thawing?

Yes. Freezing would practically stop all biochemical reactions. Household freezer can maintain -15⁰C so that would work. However, freezing also damages the cells if cryoprotectants are not used. But I guess that is not your concern.


How to categorize non-coding sequences in the genome? I'm trying to wrap my head around the diversity of functions in a genome. Obviously, you've got coding and non-coding regions. But within "non-coding" regions, it seems to be a "wild west" to me. Transposable elements, SINEs, LINEs, transposons, retrotransposons, introns, promotors, etc. Have we annotated genomes enough to have a comprehensive list of the types of non-coding sequences?

It'd be really helpful for me to have a list of the types of non-coding sequences and sub-categories (where relevant). Wikipedia seems to break out a list but the figure on the same page for the human genome doesn't match. Can anyone provide a good reference for how to categorize non-coding sequences?

Here's my likely over-simplified and incomplete categorization I could come up with. Please, for those more informed, please edit!

Noncoding sequences can be broken up into the following categories:

1. RNA genes (genes that produce tRNAs, rRNAs, miRNAs, etc.)
2. Introns and untranslated regions (UTRs)
3. Cis- and trans-regulatory elements
    3.1. Cis-regulatory elements (CREs)
        3.1.1. Promoters
        3.1.2. Enhancers
        3.1.3. Silencers
    3.2. Trans-regulatory elements (genes for transcription factors)
4. Repetitive elements (repeated sequences, repeats)
    4.1. Long terminal repeats (LTRs)
    4.2. Variable number tandem repeats (VNTRs, tandem repeats)
        4.2.1. Satellites
        4.2.2. Minisatellites
        4.2.3. Microsatellites (short tandem repeats, simple sequence repeats)
    4.3 Transposable elements (TEs, transposons)
        4.3.1. Retrotransposons (Class I TEs)
            4.3.1.1. Short interspersed nuclear elements (SINEs)
            4.3.1.2. Long interspersed nuclear elements (LINEs)
        4.3.2. DNA transposons (Class II TEs)
    4.4. Telomeres
5. Pseudogenes


Difference between intervertebral and vertebral foramina In the human spine, what is the difference between intervertebral and vertebral foramina? Is it just a matter of perspective and do they refer to the same thing or are they different?

They are actually different.

(source: emory.edu)
INTERVERTEBRAL FORAMINA is actually spaces between adjacent vertebrae which gives passage for spinal nerves to exit.
Whereas, VERTEBRAL FORAMINA forms vertebral canal.
Source:
Organization of the Nervous System: An introduction for students in the Human Anatomy Course


How do sporozoites travel into the human host when the mosquito is sucking blood? I mean how are the sporozoites able to swim in the reverse direction of blood flow through the proboscis of the mosquito into the human body?

Nice question!  Basically, the mosquito does not only suck; it also injects some saliva into the host with its saliva glands.  From National Geographic:

  The mosquito starts salivating as soon as it probes the [host]’s skin, releasing substances that prevent blood vessels from constricting, stop blood from clotting, and prevent inflammation. Sometimes, Choumet could see the saliva as small bubbles that hung around the tips of the mouthparts. And even after the mosquito stops feeding, pockets of saliva linger in the lower layers of the skin.

And from cdc.gov:

  After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

The probiscus is actually equipped to inject saliva as well as to suck blood.  And once the saliva has entered the victim, it can spread to the whole body since the blood is constantly moving.  From mosquitnoband.com:

  Mosquitoes also have special hematophagous arthropod saliva in their proboscis. Hematophagous arthropod saliva is a scientific way of saying “spit from a blood-sucking creature with an exoskeleton.” This specific type of saliva has chemicals and proteins in it that prevents blood from clotting. So what do mosquitoes do with their hematophagous arthropod saliva? They inject it into their victim before they start sucking its blood to prevent any clotting while they slurp.

Hope this helps!


Cell-autonomous viral defense involving oxidative burst? I'm looking for a mechanism by which a cell detects a virus (probably a retrovirus) within itself, then triggers an oxidative burst in response. This should all happen within the cell itself, independent of any immune-specific cells outside. Ultimately interested in humans, but any pointers whatsoever would help.

So, the cell may trigger an oxidative burst in response to pathogen (not specifically virus).
In case of retroviruses, they are hard to detect for the cell (example HIV) as they use the cell machinery for replication and can also stay in inactive latent state thereby not triggering immune response.
Hope you found your answer. Thank you and good day.


Usage and mechanism of the Bastien protocol to treat amanitin poisoning In 1971, 1974 and 1984 a French doctor Pierre Bastien (frwiki) voluntarily poisoned himself by ingestion of Amanita phalloides mushrooms in order to popularise his method of treatment of such poisoning. This method seems to have consisted of vitamin B and C injections and dosages of Abiocine and Nifuroxazide. Is this method still being practiced or has it been discouraged? What would be the mechanism of this protocol?

I know nothing about this subject, except that I can recognize edible and poisonous fungi, to the extent that it concerns me in a practical sense. However, as I have access to a range of journals through my university I thought I would see if there was anything ‘out there’ on the topic.

A recent paper entitled Amanita phalloides poisoning: Mechanisms of toxicity and treatment by J. Garcia et al. in Food and Chemical Toxicology 86 (2015) 41–55 contains a table listing the drug therapy used in a range of countries. There is no reference to Bastien in this paper and the most frequently used therapies are benzylpenicillin and silybin.

Abiocine is another name for dihydrostreptomycin and nifuoxazide is nifuroxazide is an oral nitrofuran of questionable efficiacy. So they are not identical to the agents mentioned and Bastien’s protocol does not appear to be in current use.

The impression I get from the article is that the agents used for treatment are not strict antidotes, but rather part of a strategy to treat the general effects of the poison. To eliminate the poison activated charcoal is often used.

If Bastien’s protocol really had an effect I imagine it may have acted in a similar manner to the current agents, although I have no idea what the vitamins might have been doing (if anything). Incidentally it was the subject of a letter (in English) to Lancet in 1981, in response to previous scepticism expressed in a previous editorial.


Why do men have a higher hematocrit (red blood cell count) than women? The hematocrit, also known as packed cell volume (PCV) or erythrocyte volume fraction (EVF), is the volume percentage (%) of red blood cells in blood. It is normally 45% for men and 40% for women.

so,Why do we have hematocrit for men?

First,I thought it might be caused by different hormones but I couldn't find adequate evidence to prove this Hypothesis.Therefore I decided to share it.

I found a nice article that has insights to this matter. As posted before me it is true that only adults, but not juvenile individuals show this difference. Direct and indirect effects of sex hormones on bone marrow erythropoiesis and renal erythropoietin production has been proven, but it works in both sexes the same way. Females are capable to elevate their haemoglobin / red blood cell levels to external stimuli, yet at same conditions (same altitude etc) the difference remains. Also:

  Men, premenopausal women and postmenopausal women have similar plasma erythropoietin levels, indicating that women do not attempt to compensate for their lower haemoglobin levels by increasing erythropoietic drive. These observations show that the prevailing lower haemoglobin level in females cannot be ascribed to a lack of bone marrow or renal erythropoietic capability: they indicate that adult females maintain their venous haemoglobin levels at a lower level than adult males as a physiological steady state — they do not try under physiological conditions to maintain the same levels as adult males.

This could be achieved by modulation of the juxtaglomerular apparatus signal (JGA) of the kidney. The JGA has important role in the regulation of the haemoglobin level - it is the main input for erythropoietic red blood cell production by regulating renal filtration and thus regulating the amount of oxygen that gets to the EPO producing peritubular cells.

It is noteworthy to say that similar difference exist in mammals and even there are examples among birds and reptiles.

It is described in the linked paper that both men and women achieve the same or very similar microcirculatory haematocrit level inspite the different mean venous haemoglobin levels.

This implies the very interesting theory / reasoning in the article:

  (...) that both sexes set their mean optimum level separately and to some degree independently.(...) the red cell mass is an enormous resource in animals — one third of the body's cells by number in adult humans, and demands enormous effort to establish and maintain.(...)This price must be paid for by increased fitness.(...)The excess red cells over the critical minimum that circulate in the large vessels (and slowly through in the spleen in some species) and that constitute half or more of the venous haemoglobin level probably provide a storage function for the reserve red cell mass for use when the need arises for increased work — fight, flight, food and reproduction. They may also act as reserves for heat exchange and iron storage. It is likely that the return in fitness from this reserve differs between the sexes, and therefore that the optimal size for maximal cost benefit also differs.


Why does the DSC peak have a bell shape? I am studying Differential Scanning Calorimetry (DSC) and am not quite understanding why most proteins have a bell shape when the heat capacity is plotted against the temperature.

Also, I would appreciate if you could provide good sources on this topic (books, articles, etc).

This is just a guess, but it's probably because the heat measurement is actually measuring the sum of many, many molecules reactions. It is a fact of mathematics, rather than natural science, that forces such phenomena to approximately follow bell curves (i.e., Gaussian functions). Basically, the central limit theorem states that if you have many instances of the same (random) variables and average them together, then the result will look like a bell curve. Here, the local thermodynamic change induced by a single individual protein molecule, as a function of the temperature, is presumably that random variable, since the thermodynamic behaviour of each protein is roughly similarly distributed. The randomness comes from the essentially chaotic random movements of the molecules.

See here or here for more.


Are there verbs for "undergo mitosis" and "undergo meiosis"? From my experience on SE sites, I believe this is the right site to ask this question under "terminology".

I've been trying to find out whether English has one-word verbs for "undergo mitosis" and "undergo meiosis". I haven't been able to find confirmation on Google, but my linguistic imagination is limited, and I may have failed to google the right things.

Could you tell me if there are such verbs in common use in biology? I mean, if such verbs exist, can I find them in modern biology books or papers?

I'm actually not sure myself. If I were to use something, I would go with "Mitos'd" and "Meios'd".

However, you may not win over many fans, depending on the audience. If it's with students or maybe a professor, you could get away with shortening the processes. If it's in any formal setting, be as precise and descriptive as possible. It's not a lot of trouble to be more accurate and add "underwent" to the sentence.


What is the essential benefit of center-surround organization of retinal ganglion cells? I am trying to understand the significance of the overlapping on-center off-surround and off-center on-surround organization of the retinal ganglion cells, also called center-surround organization. What is the advantage of such an organization from the point of view of vision?

To highlight the point of the question, wouldn't it be computationally and organizationally easier to simply have the retinal ganglion cells arranged in a non-overlapping fashion, and without the center-surround ability? Then there would be a straightforward correspondence between the incoming spots of light and the firing of adjacent neurons in the optic nerve.

You are assuming that light comes in perfectly in spots, and that the purpose of vision is to replicate a "bitmap" of the incoming light. This would actually be very inefficient computationally.

In reality, vision relies on detecting salient features. Imagine a simple scene, maybe like this one:

Most of the white space of the wall is pretty uninteresting: you have no need to really process that information besides knowing it's one solid area. What is interesting in the image, if you are trying to understand the space your are occupying, is to see the edge between the floor and the wall. In fact, that's what really tells you this is a wall and a floor: if you only had the upper 1/4 of the image, you would just have a white box: you wouldn't know if this is a floor, a wall, a ceiling, the paint on someones car. The edge between the floor and wall gives you the needed context.

Lets think about how center-surround organization would respond to this image. In the whole blank white space, white light is hitting both the center and the surround: these cancel and there is little response. However, imagine what happens for an on-center off-surround cell right at the edge with the floor. That cell is getting white at its on-center, but only on about half of it's off-surround: the other half of the off-surround instead gets the darker wood floor. This cell would therefore respond to the imbalance in the average surround vs average center!

You can then combine many of this circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception

Note: the LGN (thalamus) receptive fields are very similar to the retinal ganglion cell receptive fields. In V1, primary visual cortex, these receptive fields are added together to make "simple cells" which respond to edges.

I think this picture comes closest to answering your question about how overlapping receptive fields can be useful.

This image from the Wikipedia page on receptive fields shows what you get when you put a scene through a center-surround filter: note how all the edges are emphasized!

Other benefits: this type of detector works well over a range of light levels, for example different steps of gray will appear the same, even though the pixel intensity varies a lot. This way, you get similar responses to edges in both a dark and light room. These detectors also help to sharpen images. Note that computer vision uses some of these same strategies as well!

What if you wanted to detect spots of dark instead of spots of light? We often think of eyes as being "light detectors" but they are just as appropriately described as "dark detectors." Imagine you are a rodent looking up at the sky, for example: an important, salient stimulus for you might be a dark spot where a hawk is blocking light from the sky. Therefore, having an off-center, on-surround type of cell is just as useful as the opposite (and indeed, the retina contains both types of retinal ganglion cells).


Why was the cackling goose split off as a distinct species from the Canada goose in 2004? According to Wikipedia, in 2004 the American Ornithologists' Union made the cackling goose a new species, splitting it away from the Canada goose.  The British followed suit in 2005.

What was the basis for this split?  Why was a new species required here?  Were offspring of these two found to be consistently infertile, or was the change based on something else?

The "white-cheeked" geese have long been subject to taxonomic controversy. From the 1920s to the 1950s, authorities have classified them into between one and four species. Although Aldrich in 1946 asserted there was near-unanimous agreement among Arctic biologists that there were two species, from the 1950s Delacour's taxonomy was most often followed, which had one species (Branta canadensis) and twelve subspecies.(1)

What changed the consensus were DNA studies.  Mitochondrial DNA (mtDNA), which is passed on without recombination, showed distinct sequences supporting two species. One RFLP analysis of mtDNA suggested the split between these two species happened about one million years ago.(1)

The species divide mainly along size and breeding location lines.  The Cackling Goose (Branta hutchinsii) is smaller and breeds on the Arctic tundra. The (present) Canada Goose species (Branta canadensis) mostly takes a larger form and breeds mostly in non-tundra areas.(1)

(1) - Mlodinow, S. G., et al. "Distribution and identification of Cackling Goose (Branta hutchinsii) subspecies." North American Birds 62.3 (2008): 344-360.


Why do large, aromatic residues prefer beta-pleated sheets? I read in many journals that amino acids with branched and large aromatic R-groups have higher beta pleated sheet propensities. However, none really go in depth into the significance or reasoning behind this finding. I have made an educated guess based on my findings on alpha helix propensities:
In alpha helices, branched and aromatic R-groups are not favored as the g+ and g- isomers can extend into the helix and interfere with the hydrogen bonding. In beta pleated sheets, however, the R-groups are pointed perpendicular to the hydrogen bonds, and even large R-groups like that of phenylalanine or tryptophan will not able to reach the site of hydrogen bonding. Coupled with the fact that smaller amino acids will rather be more tightly bound to each other (so they prefer helices, e.g. collagen helix, alpha helix, save space, amide hydrogens and carbonyl oxygens closer together), larger amino acids therefore favor formation of beta pleated sheets.
I need a few key pieces of info to really accept my own explanation (if it is correct) as factual. First, I will need proof that beta pleated sheets are more structurally rigid than alpha helices (or else, smaller R-groups like that of alanine and cysteine will also prefer beta pleated sheets). I also kinda want to see the structure of beta pleated sheets with large R-groups to further ground the thought in my head, as I can't really see how R-groups like valine (heavily branched) will not affect hydrogen bonding. As an example, I attach one that I found for alpha helices.

This table is from the Wikipedia page for α-helix:

As you can see aromatics are not the worst offenders. In fact, barring proline (whose backbone torsion angles are unsuited to helices), Gly is the worst offender. A likely reason for this is Gly being too flexible i.e. its small side chain H allows it to adopt backbone torsion angles unsuited for α-helix.
As another example let's look at silk, an extended anti parallel β-sheet structure, from libretexts.

As you can see, the small side chains of Ala and Gly in fact allows the β-strands to come close enough to form backbone hydrogen bonds. In fact, from the same reference I quote - "Unlike the α helix, though, the side chains are squeezed rather close together in a pleated-sheet arrangement. In consequence very bulky side chains make the structure unstable."
So it is not entirely true that aromatic amino acids prefer pleated β-sheets.
So what are we missing? We are missing the chemical environment in which the the amino acid residues are placed. Remember, most of the propensity charts we look at are average propensities across known protein structures. In a specific protein, its specific chemical context can radically change the secondary structure propensities.


Do Asian koel males communicate through calls? Male Asian koels are heard making long koo-Ooo s  which are returned by similar koo-Ooo s1 from some far away place. While the female makes short shrills.

I never had the opportunity to see the other bird and find out its sex. But it sounds just like the first one.

Is it actually communicating with a male bird? What is the known reason if so?

1 The reply calls (to be found around 0:29) in the video are really low.

Note:

A singing male bird also gives desperate accelerated calls when  mimicked.
Its breeding season has just begun in India and this communication can be heard.

Still working on this question and the following are the findings:

The male bird when mimicked possibility mistakes the mimic as an intruder in its territory and so it gives louder & accelerated calls.

  The male while defending its territory gradually approaches its adversary, hopping from twig to twig calling loudly and displaying its threatening posture. ( B S Lamba (1969) )


Homework - Genetics linkage problem A farmer purchases f1 hybrid seeds. These seeds contain four heterozygous loci that give a significant increase in crop yield when compared to either homozygote. Two of these loci are on the same chromosome and show partial linkage. If the farmer allows the f1 plants to self-fertilize, what is the probability that a seed from the resulting f2 generation has all four heterozygous loci?

a) at least 1/2

b) between 1/2 and 1/4

c) between 1/4 and 1/8

d) between 1/8 and 1/16

e) less than 1/16

I think it's either d or e. For the first two genes (unlinked), there is 1/2 chance to get heterozygote. So, 1/2 * 1/2 = 1/4. For the next two linked genes, if they were unlinked, it would be 1/2*1/2 = 1/4 for a total of 1/16. But since they are linked, I'm thinking that the chance for heterozygote might be reduced, so maybe the answer is e) less than 1/16?? Not sure where to end, though...

I agree with your reasoning! If the two genes are perfectly linked, then the answer is $\frac{1}{8}$. If they are perfectly unlinked, then the answer is $\frac{1}{16}$. The answer therefore must be somewhere between $\frac{1}{8}$ and $\frac{1}{16}$.  Good job!

Of course the answer e) is pretty silly as any other answer ('a','b','c' and 'd') would yield to 'e' being necessarily true. So, if you have to choose only one, I would just go with 'd' and highlight that the answer 'e' is silly.

  I still don’t understand how if the two are completely linked, the answer would be 1/8.

Let's consider that at both loci, we have two alleles A and B. Here is a representation of the first F1 individual

-------A----A-----
-------B----B-----

Here is a representation of the second F1 individual

-------A----A-----
-------B----B-----

Of course, they are the same as the parental lines are pure breed. Now, if the two loci are perfectly linked, then the offspring can have the following possible genotypes

-------A----A-----
-------A----A-----,

-------B----B-----
-------A----A-----,

-------A----A-----
-------B----B-----

or

-------B----B-----
-------B----B-----

, but the offspring cannot be

-------B----A-----
-------B----B-----

or an other combination requiring recombination between the two loci. Therefore the probability to be heterozygote for the F2 at two perfectly linked loci is the same as the probability to be heterozygote at one of these two loci (if we assume the mutation rate is negligible).

  Why can't parents be: parent1: -------B----A----- -------A----B----- parent2: -------A----A----- -------B----B-----[?]

Because parental lines are pure lines. When we talk about an F1 generation, we talk about the hybrid between two pure line. By pure line, we mean that we got rid of all genetic variance. So, one parental line is fixed for the A alleles and the other line is fixed for the B alleles.  In other words here are the genotypes of the pure parental lines.

-------A----A-----
-------A----A-----

and

-------B----B-----
-------B----B-----

One parent can therefore only give

-------A----A-----

while the other one can only give

-------B----B-----

so, the F1 generation is therefore necessarily heterozygote at all loci.