Classification of glycosidic anomeric bonds (alpha vs. beta) In the process of studying for my upcoming biochemistry exam, I have stumbled over the classification of glycosidic bonds. I want to be able to distinguish $\alpha$- from $\beta$-glycosidic bonds. Unfortunately, even after reading through this page, I don't really understand how to go about classifying the bonds in e.g. an oligosaccharide.

(Source)

Now, I am inclined to say that both of these anomeric linkages are of type $\alpha$, because the O-glycosidic bond is axial to the respective sugar rings. Is that a correct way of reasoning?

Here's my interpretation, as far as I can get, which agrees with your deduction that both of the O-glycosidic bonds involve α epimers. (If the epimeric carbon has an -OH in the axial direction then this is the α anomer.)

Do you have the name of this compound?

Let's hope that a real glycobiologist comes along.

Supplementary
I'm now not sure that it is even possible to assign an anomeric state to the sugar marked as ?. There is no indication in the diagram of the presence of a -CH2OH substituent on the ring - it appears to have a methyl group instead. If that group was a -CH2OH then the putative anomeric C would indeed be in the α form since it is pointing in the opposite direction from the "-CH2OH" (c.f. the two galactose residues). If ? is a deoxy- derivative of a sugar then it may be that the convention still holds.


Are ectopic beats considered sinus rhythm for pNN50 purposes? One quantification of the heart rate variability of an ECG is pNNx, i.e. the proportion of consecutive NN distances that differ by at least 50 ms. When a premature beat occurs, the preceding and following RR intervals are much shorter and longer than the mean. Are these intervals considered NN for the purpose of calculating the pNN50?

No, the beats originating outside of the sinoatrial node are not considered for pNN50. Moreover, this metric cannot be applied to the rhythm featuring any type of ectopic or non-sinoatrial activity.

NN50 has its name from an acronym "normal-to-normal", this acronym is used instead of RR ("from R to R") to emphasize that only the normal, e.g. sinoatrial beats are considered for evaluation.


Can dead scorpions still sting? I found a dead scorpion on the sidewalk today, and brought it home, being careful not to touch its stinger. Bees can sting even after they are dead, if you step on them in such a way that it pushes their stinger out.

Does the same apply to scorpions?  Do I need to be careful not to touch its stinger?

Yes, the bark scorpion can still sting after death. I learned this myself after stepping on one. As I make a nightly habit of patrolling inside my home for their presence, I can conclude the offender had died within 12 hours of my stepping on it. When they die their tails stretch straight behind their bodies, this was the position I found it in.


How do these triplets code for these proteins? I am slightly confused by the diagram above.

The first codon of the unaltered DNA is AAG. During transcription, isn't this coverted to UUC (mRNA). So doesn't UUC code for phe and not Lys?

Likewise, how does TAG code for a stop codon? Isn't it transcibed to AUC, which codes for ile?

Also, is that the coding strand or template strand? If there is a mutation in the coding strand, is there any impact on the protein?

In the first image, AAG is the true codon for Lysine.  So when the ribosome hits "AAG" in the mRNA it recruits a Lysine-tRNA.

What can be confusing is the use of the term "coding strand" when talking about the DNA. The coding strand is illustrated in the second image you posted, and it is the coding strand of DNA that the first image is depicting. What "coding strand" means here is, this is the strand that looks like the mRNA will look. Depicting the DNA coding strand like this--i.e. as a series of codons--can be slightly misleading since we know codons really only mean anything when in the form of mRNA. Nevertheless, it is a common way of thinking about DNA.

Back to the first image. Because it is showing the "coding strand" of DNA, the "template strand" for 5'-AAG-3' then must be 5'-CTT-3'. Hence, when this strand is transcribed by RNA polymerase, the 5'-CTT-3'(DNA) becomes 5'-AAG-3'(mRNA).


The meaning of the "Score" in ScanProsite I'm doing some research about a proteïne which is sequenced, however Í'm not able to find any information about the score which ProSite scan shows after finding an possible domain profile.

I have read the prosite help, however there isn't anything which explains what the score means.

The score provides an indication of well a specific profile (which is a weight matrix) matches the profile for the domain. Section II.B. Profiles development explains this in further detail.

A paper that outlines the development of PROSITE notes that they primarily use a cut-off of 8.5 and explains the score thus;

  the raw scores in PROSITE profiles are converted into so-called ‘log10
  per residue E-values’, allowing the computation of the number of
  expected matches with equal or higher score in a database of a given
  size. For instance a match with a normalised score of 9.0 or higher is
  expected to occur about once in a database of one billion residues.


Is there a Reverse Transcription optimization for long, 9kb, transcripts? Has anyone optimized RT for long transcripts (9kb)? The downstream application will be PCR amplification and Illumina library prep.  It will be trivial to make internal primers sets for the PCR that are specific as long as there are no chimeric sequences.  If there are, they will probably get primed also.  If anyone knows of an optimization and/or other potential pitfalls, I would love to hear them.

RT-PCR should be able to get you up to ~10kb. If you are finding that it is not working, then you can by long-range RT-PCR kits commercially (look at Stratagene and Qiagen, for example). The Qiagen can handle up to 12.5 kb in a two-step RT-PCR system.


How non-invasive blood glucose concentration measurement work? Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.

Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping onto the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

This is not a new thing, by checking the articles about non-invasive glucose level measurement, it started in the early 90's.

  Near-infrared (NIR) spectra of the human inner lip were obtained by
  using a special optimized accessory for diffuse reflectance
  measurements. The partial-least squares (PLS) multivariate calibration
  algorithm was applied for linear regression of the spectral data
  between 9000 and 5500 cm−1 (λ = 1.1-1.8 μm) against blood glucose
  concentrations determined by a standard clinical enzymatic method.
  Calibration experiments with a single person were carried out under
  varying conditions, as well as with a population of 133 different
  patients, with capillary and venous blood glucose concentration values
  provided. A genuine correlation between the blood glucose
  concentrations and the NIR-spectra can be proven. A time lag of about
  10 min for the glucose concentration in the spectroscopically probed
  tissue volume vs. the capillary concentration can be estimated.
  Mean-square prediction errors obtained by cross-validation were in the
  range of 45 to 55 mg/dL. An analysis of different variance factors
  showed that the major contribution to the average prediction
  uncertainty was due to the reduced measurement reproducibility, i.e.,
  variations in lip position and contact pressure. The results
  demonstrate the feasibility of using diffuse reflectance
  NIR-spectroscopy for the noninvasive measurement of blood glucose.

1993 - Noninvasive Blood Glucose Assay by Near-Infrared Diffuse Reflectance Spectroscopy of the Human Inner Lip

There are multiple approaches, mostly spectroscopy, but dielectric properties (e.g. conductivity) can depend on glucose levels too. Saliva can be used to measure glucose levels as well.

2014 - Non-invasive glucose monitoring using impedance spectroscopy
2014 - Broadband Tissue Mimicking Phantoms and a Patch Resonator for Evaluating Noninvasive Monitoring of Blood Glucose Levels
2014 - A paper strip based non-invasive glucose biosensor for salivary analysis

The details of each technology you can find of wikipedia.


Can anyone identify this locust / grasshopper in Florida, USA? Found in Pinellas County, Florida

It appears to be Romalea microptera, or the eastern lubber grasshoper, which is commonly found in the southeastern United States, including Florida.

https://en.wikipedia.org/wiki/Romalea_microptera
http://eol.org/pages/965190/overview

Photo by Steve Smith.


Why can't amylase break down glycogen? Amylase is an enzyme that breaks down starch in the form of amylopectin and amylose. Both amylose and amylopectin are formed by alpha glucose joined together by (1-4) and (1-6) glycosidic bonds. Glycogen is no exception, just that it has more branching. However, why is it that a google search shows that it is hydrolyzed by Glycogen Phosphorylase rather than amylase? Also, how can amylase digest both (1,6) and (1,4) glycosidic bonds?

Any help would be greatly appreciated.

At an approximation the active sites of enzymes can be considered as having two aspects. The first relates to the catalysis — in this case the breaking of the glycosidic linkage. The second relates to binding the substrate. This review of the α-amylases by MacGregor et al. shows that there is a range of a-amylases, differing in this latter respect — their substrate specificity. In general there are binding sites for a varying numbers of glucose residues at either side of the bond being cleaved. This is shown in Fig. 3 of that review:

The important difference in the structure of glycogen and starch (amylopectin) — seldom mentioned in general biochemical or biology texts — is their patten of branching:

As this previous answer of mine to a different question explains, this results in a globular structure for glycogen granules in which only the ends of the chains are accessible. (The image below, from Protopedia, illustrates this better, especially if you imagine it in three dimensions.)

Hence the substrate-binding site of α-amylase does not have access to the residues that need to bind for it to perform hydroysis of glycogen, and, indeed, the enzyme that breaks down glycogen — glycogen phosphorylase — is specific for these free ends.

The α-amylases that can hydrolyse both α-1,4 and α-1,6 glycosidic links are quite few compared with those with specificity to one or the other type of linkage (see Table 2 of the MacGregor review, if you can obtain access to it). The impression obtained from following up two of the examples there is that the enzymes involved can exist in alternative conformations, the correct one of which is triggered by the substrate. An example is the glycogen debranching enzyme, the studies of which in Sulfolobus solfataricus and Candida glabrata can be read freely on-line. Although somewhat less directly relevant, the example of a Thermoactinomyces vulgaris neopullulanase is another variation on this theme.


Animal with "advantageous" trait in a environment where the trait is never utilized (high cold tolerance in mild climate) - natural selection occur? If you were to put an animal with a certain type of seemingly advantageous "trait" into an environment where the trait was not necessarily needed, ex: Putting an animal with a high tolerance for cold into a mild climate, what kind of natural selection occur? Balancing?

Recipe for selection

There is selection on a specific phenotypic trait if and only if

There is variance for this trait in the population
This variance is, in part at least, explained by genetic variance
The trait covaries with fitness

The first two points can be reduced to a single point by stating "The trait has some non-zero heritability in the population". For more information about heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

This recipe is often called Lewontin recipe.

Applying the recipe to your case

So, in the model you consider, some individuals are cold tolerant and some aren't, so the first point is checked!

We will assume that the difference in cold tolerance is caused by genetic differences. Second point is checked.

Does the trait covary with fitness? As you defined that, in the environment considered, being cold tolerant does not have any impact on fitness, then no, there is no covariance between the trait and fitness. The third point is not checked and therefore, there is no selection happening.

Are you sure there is no cost to being cold tolerant?

Note, btw, that it is not rare to observe (or at least to assume) that some adaptation such as cold tolerance would come at a comparable cost when the environment is warm enough.

For example, increased cold tolerance might be mediated via anti-freeze proteins. The production of such proteins might be costly for the individual. In such case, we would have a covariance between fitness and the trait (cold tolerant individuals would have lower fitness that individuals that are not cold tolerant) and hence selection should act as to reduce the frequency of individuals that are cold tolerant in the population (always assuming an environment that is warm).

What else could cause the frequency of cold tolerance to evolve?

In absence of selection, the frequency of cold tolerance individuals might still evolve in the population. Things like genetic drift, selection at linked site or selection at correlated trait or migration can typically affect this frequency.


How does the brain fake itself into hearing our own sounds even when we are not speaking? Typically When we are talking to our own selves at any time in the day,the Brain thinks that it's me who's speaking , how does it create illusion of speaking ?

Our brains treat 'talking to ourselves' very similarly to talking to others. There's a small amount of evidence in studies to suggest that when we talk to ourselves, it's like verbalising the speech out loud.

Before you speak out loud, the part of your brain responsible for creating speech copies that information, and moves it the appropriate verbalising areas of the brain. However, at the same time in a process called efference-copy, it also copies it to the area of the brain responsible for listening to sounds. This process overall means that our brains can distinguish sounds that come from ourselves, and sounds that come from other people.

This also partially goes to explain why people with schizophrenia have difficulty recognising their own internal voices as 'own'. It's likely that this process has gone awry in these people, meaning they're not able to recognise their internal voice as themselves.

Here's a link to some research done in Sydney on this matter.


If mammals evolved to be nocturnal, then how did we get so staunchly diurnal in such short time? Much of human health revolves around sleeping well through the night.  We know about circadian and body temperature rhythms which make us sleepy at night, peak melatonin production in the middle of the night, deep sleep phases, sleep disruption from light at night, and high cancer rates among people who work the night shift.

Clearly, we are built to sleep at night.  You would suppose, then, that we must have evolved to be diurnal long ago and descend from a long line of diurnal animals.

Yet, the evolutionary legacy of mammals is predominantly nocturnal.  Mammals started out as nocturnal (to avoid the reptiles) and most mammals today are still nocturnal.

How did we get so staunchly diurnal so quickly?

The Nocturnal bottleneck for mammals as it's called was assumed 'til recently to have only ended at the Cretaceous–Paleogene extinction event 66 million years ago.

At the basis of the nocturnal bottleneck hypothesis lies the idea that
Mesozoic ectothermic reptiles (including dinosaurs) would be
restricted to daytime activity at times when the sun can help to heat
up their body to operating temperatures.......

The arguments against:

include:

(i) presence of insulating proto-feathers,

(ii) fossils of breeding dinosaurs in cold regions

(iii) raised body posture

(iv) fibrolamellar bone structures

(v) presence of nasal turbulate bone structures

(vi) stable growth rate (isotope deposits in bones and teeth)

(vii) possible ‘mass homeothermia’ or ‘inert homeothermia’ in large dinosaurs

(viii) the occurrence of small dinosaurs in cold regions

(ix) the existence of potential external thermoregulatory structures in some dinosaur species (e.g. dorsal boney plates in Stegosauria).

Recent molecular analyses have added to the doubt of the original theory:

saurischians are now generally believed to have had partial
endothermia, allowing them to incubate their eggs and inhabit colder
regions......
Independently, parallel evolution in Synapsida led to partial
endothermia in therapsid reptiles (250 Ma, Late Permian) and full
endothermia in mammals

Nespolo RF, Bacigalupe LD, Figueroa CC, Koteja P, Opazo JC. 2011. Using new tools to solve an old problem: the evolution of endothermy in vertebrates. Trends Ecol. Evol. 26, 414–423
The implication being that the pure nocturnal adaptation in mammals would not be a completley effective strategy for predator evasion.

In a large comparative study [Roll], divided 700 species into classes of
dominant temporal activity niche: nocturnal, diurnal or both (mostly
crepuscular). They used an existing phylogenetic construction to
reconstruct the evolution of diurnality in rodents, which are thought
to have diversified after the K/T boundary. The reconstruction of
temporal niche usage within rodents led to the conclusion that rodents
shared a nocturnal ancestor that existed before the K/T boundary.
Subsequently, diurnality evolved through secondary evolution at least
seven times independently in Rodentia.
Using the molecular phylogenetic construction of [Huchon et al],
we constructed the temporal niche phylogeny within the full therian
subclass using the nocturnal, diurnal and
crepuscular/arrhythmic classification of [Roll et al.]. The most
parsimonious interpretation leads to a minimum of 16 changes of
dominant temporal niche.

Bolding mine.

Most subdivisions of Theria are indeed nocturnal, but many changes and reversions occurred, and different interpretations may be
possible, especially when higher-quality data on activity patterns in
more species become available.

Conclusion.
It apears that mamals may have been chased by the saurischians throughout the day, night and twilight hours and that many adaptations and reversions may have occured over a period (possibly) much longer than the 66 million years previously thought. Research is ongoing.
Bolded references:
Roll U, Dayan T, Kronfeld-Schor N. 2006. On the role of phylogeny in determining activity patterns of rodents. Evol. Ecol. 20, 479–490
Huchon D, Madsen O, Sibbald MJ, Ament K, Stanhope MJ, Catzeflis F, de Jong WW, Douzery EJ. 2002. Rodent phylogeny and a timescale for the evolution of Glires: evidence from an extensive taxon sampling using three nuclear genes. Mol. Biol. Evol. 19, 1053–1065


Found a larva in my broccoli, is it a Small White (Pieris rapae)? Found this living larva in broccoli from a store. It was about 10 mm long. It was in july this year, and I don't remember the country of origin for the broccoli. A bit of googling makes me think it could be a Pieris rapae, but I don't know if there are any similar species.

edit: Even if I don't know the origin of the broccoli, I assume (and hope) it was grown in Europe since I got it in Sweden.

It definately looks like a Pieris rapae larvae, which are distinct from larvae in closely related common species as e.g. Pieris napi and Pieris brassicae. However, I'm not a lepidopterist and there might be related rarer species I'm not aware of, especially since you don't know where the broccoli is from. However, Pieris rapae is found basically all over the world as native or introduced (native in Europe, Asia, Africa and introduced in e.g. Ameria and Australia) and is a pest species of cabbage (including broccoli) so it is a very good fit.


Do any known viruses contain "junk" or parasitic genomic information? After reading about so-called "mystery proteins" in this excellent summary of the coronavirus genome (and acknowledging that the "mystery" simply reflects our lack of knowledge about a very new virus), I'm curious if any known viruses can contain parasitic genetic information "along for the ride", or if their genomes are selected, generally speaking, to be as informationally efficient as possible, for what is encoded? In other words, does selection pressure allow for these parasites to contain their own parasites, and are there known examples of such, if so?

I'm curious if any known viruses can contain parasitic genetic information "along for the ride"

Analogous to the parasitic transposons mentioned in the paper linked by canadianer, phage-inducible chromosomal islands are mobile elements that "hijack" the molecular machinery of bacteriophage during lytic infection of Gram-negative hosts.  PICI elements, as they're called, encode Rpp proteins that complex with the phage TerS homodimer, changing the conformation of the complex such that the PICI cos mimic is preferentially bound and packaged into the empty capsid.  Fillol-Salom et al. 2019 1 discuss in detail the mechanism of PICI propagation and provide a good graphical abstract of the process:

Similar elements exist in Gram-positive bacteria, specifically Staphylococcus aureus, called Staphylococcus aureus pathogenicity islands (SaPIs).  Instead of encoding a separate protein that complexes with the phage TerS, SaPIs encode a homolog of TerS that specifically recognizes and packages SaPI DNA into phage capsids.2
Note that this answer does not directly address the question of "junk" DNA in viruses, as PICI elements are dormant in the genomes of the bacterial hosts rather than the genomes of the viruses themselves.  Though, I believe this is relevant insomuch that they parasitize bacteriophage, and are therefore "along for the ride" in the viral capsid.

Citations

Hijacking the Hijackers: Escherichia coli Pathogenicity Islands Redirect Helper Phage Packaging for Their Own Benefit
Role of Staphylococcal Phage and SaPI Integrase in Intra- and Interspecies SaPI Transfer


Why doesn't it feel suffocating when taking a shower? When one walks into a bathroom where someone is (or just finished) taking a shower it is hard to breathe, because it's filled with steam, yet the person taking a shower can breathe just fine despite being in the area with even more steam.

Why is that?

Most likely a matter of relative perception.

For example, if you start with empty hands and pick up a 20 pound weight, you will perceive it as heavier than if you start with a 10 pound weight and then pick up a 20 pound weight.

Likewise, whoever's in the shower had plenty of time to get accustomed to gradually increasing steam, while you walked in and got the full blast immediately.


Do smaller intelligent animals have a higher neuron density to account for their seeming intelligence? Otherwise, what? It seems like there's a lot of very small animals that have a much higher intelligence than what you would expect if you linearly projected intelligence as a function of brain size. There's ravens, crows and parrots which are much smaller than humans but have a recognizably high intelligence and emotional capacity. Then there's rats and general rodents like squirrels or similar animals like raccoons, and I guess an octopus to throw in which are good at problem solving and fierce fighters. Then there's also bugs like ants which are somehow very versatile and can adapt to many situations despite being that tiny, and with recent information may also have a recognizable emotional capacity like possibly bees.

It would make sense to me if the correlation between neuron density and intelligence isn't linear, but I don't have the information to make any determinations.

It also may be the case that we are implying intelligence in some cases.
The responses these animals show may have been evolutionarily selected as it best for their survival. However, to us the benefits of these responses may not be directly visible. For example, sheep herding dogs may have a high degree of spatial and numerical capabilities since humans bred them for these traits.


Interesting examples of models I am studying the general use of models in biology in terms of methodology, applications, usefulness etc, and I would really appreciate any recommendations of some specific examples of models from any area in biology. Some examples are the logistic growth model or the Lotka-Volterra prey predator model.

It would be nice if you could shortly explain what the model is used for and why do you think it's an interesting case, and give a reference for further study.

Also any recommendation of books on model development and other meta-model questions in biology is very welcome. Thank you.

Biology is a large field of knowledge! As you give examples drawn from population biology (logistic population growth and Lotka-Voltera models), I will assume you are mainly interested in ecology and evolution.

For analytical models used in ecology and evolution, I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Day. The book assumes a relatively low level of knowledge in mathematics from the reader and walk the reader through most of the most iconic models in ecology and evolution, their analysis and interpretation. The mathematical tools used in this book include linear algebra, equilibrium analysis, analysis of cyclic behaviour, Markov chain and esp. birth-death processes, diffusion equations, probability theory and stochastic models, approximation theory, class structure models (Leslie matrix and more) and, separation of time scales among others.

For books, mainly theoretical, in population genetics, please have a look at the post Books on population or evolutionary genetics?.

As you talk about the Lotka-Voltera model, you will find an intro to this model in the post What prevents predator overpopulation?.


Where can I find clinical trial data published in JAMA? Data in the paper:

http://jama.jamanetwork.com/article.aspx?articleid=336799

is cited in the statistical analysis in the book Clinical Trial Data Analysis using R. Can anyone help me find it?

Online repository

Today, most journals (although t may depend on the field) require author to upload their data. The paper you are interested in was published in 1967 (internet was invented in 1969). It is very likely that the data have not been uploaded. It is also possible that the data have never been compiled numerically but is only on paper.

Ask the authors

Your best chance is to contact the authors directly and politely ask if they can give you their data. The author might be hard to contact as well as they may have changed university, be retired or even dead.

Possible loss of data

If you can contact the authors, then it is not unlikely that the data have just been lost. The loss might be due to a flood, to a technical issue or just because they don't know where it was placed.


What made this pile of tiny poops at the base of an old oak? Eastern Long Island, NY I ran across three trees (all with cavities) that had mounds of these small droppings at their base. These were approximately 50-100 meters from the shore of a salt marsh on the east end of long island.
We don't have porcupines, and I've never seen such piles associated with squirrels, so my first thought was bats. Any ideas?

UPDATE: I was not paying close enough attention to size. If the feces is as small as the OP mentions in the comment below this post ("20+ of these scat in an acorn"), then this is very unlikely porcupine!! Instead, the size and shape suggests the feces belong to either a rat (perhaps wood rat) or some type of squirrel.

I await an update form the OP with more specifics before diving deeper...

Hollowed-out tree? Pile of pellet-like feces? End of Winter/start of spring?
Almost assuredly these belong to a porcupine.

 Source: user Thomas at http://livingprimitively.com/2012/05/
The North American porcupine (Erethizon dorsatum), which can be found throughout Canada and much of the northern US, is present in New York.

 Source: NH PBS

Animaldiversity.org suggests that porcupines are primarily tree dwellers in the state of NY.

For a suburban example like yours, see here.

Although porcupines do not hibernate, they reduce their range significantly during the winter and will tend to accumulate large piles of scat in and near their winter den (or suite of dens -- source). Although caves are ideal as they keep porcupines warmer, they also will frequently use hollowed-out trees as winter dens.
Since the inner bark of trees is a favorite food of porcupines (source), they will linger quite a bit around their den tree or other nearby trees if available.
Porcupine scat matches what you've found. Scat is oblong, slightly curved, and composed mostly of sawdust (due to their high wood diet) [Source: here]. According to Northwoodguides:

Wood fibers are evident in their scat. Scat may be piles of pellets varying in length from 1/2 to 1 inch long or it may be present in a chainlike pattern connected by wood fibers. Color varies from season to season depending on diet but is usually brown to black.

This site also has some good info, photos, and videos.

It is unlikely your scat belongs to another mammal such as a flying squirrel. Although flying squirrel poop looks similar and is smaller, their feces will not be notable woody as they eat lichens, fungi, berries, leaves, and other non-woody foods. Source. This site suggests that flying squirrel scat can accumulate at the base of a tree, but I have not seen this nor do the other characteristics match your almost textbook example of a porcupine "poop tree."


What does "substoichiometric amounts" mean in the context of molecular biology? Recent paper:

  PRC2 is composed of the histone methyltransferase EZH2, EED, SUZ12,
  and the histone binding proteins RBBP4 and RBBP7. JARID2, AEBP2, PHF1,
  MTF2, and PHF19 are also present in PRC2 in substoichiometric amounts.

Does this have a more specific meaning than "very little" or "very small amounts", which I presume is what it means?

Paper (paywalled): http://genome.cshlp.org/content/26/7/896.abstract

It possibly refers to fractional stoichiometry i.e. less than a molecule of these proteins per molecule of PRC2. Obviously, you cannot have half a molecule and this statement means that in a gross sample, the concentration ratio of these proteins with respect to PRC2 is less than 1:1. At a molecular scale, it would mean that these proteins may not be always associated with PRC2.

This is also in agreement with the known fact that PRC2 core components are EZH2, EED, SUZ12 (along with RbAp46/48) and the others are accessory factors (Margueron and Reinberg, 2011).


Atelectasis due to decreased surfactant in lungs Surfactant is a protein lipid mixture produced by alveolar pneumocytes composed of Dipalmitoyl Phosphatidyl Choline lipid, apoproteins and calcium ions.
This surface lines the alveolar epithelium thereby reducing surface tension preventing lungs from collapse.
Atelectasis is collapse of lung mainly due to lack of surfactant.
Moreover it may also be due to obstruction of the airway tract.

My question is why is this surfactant found to be lowered in patients who have undergone cardiac surgery under pump oxygentor? Why does long term exposure to 100% Oxygen affect the surfactant.
Is it due to its chemical composition or is it something to do with pulmonary circulation?

This Wikipedia article states alveolar collapse due to Oxygen Toxicity
http://en.m.wikipedia.org/wiki/Oxygen_toxicity

Long-term exposure to excessive oxygen will lead to damage in pulmonary tissue. This damage resembles the same damage which is seen in patients with Acute Respiratory Distress Syndrome (ARDS). In these patients surfactant specific proteins are damaged by proteolysis. This proteolysis is caused by the neutrophil elastase enzyme, after a massive influx of activated neutrophils.

The damage done by exposure to excessive oxygen is thought to be done by Reactive Oxygen Species (ROS).

  Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen...

These ROS can cause oxidative damage to DNA, RNA and proteins. They can form covalent bonds between molecules in the surfactant, thus inactivating them. Damaging of molecules can lead to cellular damage, causing ROS-mediated necrosis or apoptosis. Therefore there will be less surfactant production possible.

Also interestingly:

  An important feature of pulmonary oxygen toxicity is that it is almost impossible to distinguish from damage caused by other lung injury processes. Consequently, it is unclear whether deterioration of lung function during high concentration oxygen therapy is due to worsening of the primary disease process or to oxygen-free radical-induced damage; the administration of high concentration oxygen may be perpetuating lung injury in some patients.

So in patients who undergo long-term 100% oxygen exposure, for example due to lung problems, the problems could be perpetuated or even worsened due to oxygen therapy and the oxidative stress caused by it.


Hela live cell confocal laser scanning - reccommendations for good fluorophore that will show good movement I've been doing a lot of live cell imaging lately mostly using hela cells expressing some EYFP based chimeric proteins. I'm building a video library for an art student here at the university who is going to create an exposition using the videos. I need a lot of content to make this sucessful and rather than requiring much scientific merit these videos need to be "busy" and look good. I'm looking for suggestions as to any dyes or fluorophores, drug treatments or conditions someone has worked with that will show significant movement/change of/in the cell, change in intracellular localization....doesn't matter it just needs to be a significant alteration for the cell.

I'm still really optimizing the system with the CO₂ etc.. and the longest aquisition i have taken is about 8 hours - after that either the cells are dead or the focal drift becomes too much of a problem. I am hoping to see some division once I can get the system recording long enough. Until then was looking for some suggestions as to other possibilities.

The various dyes I have been using include:  hoechst, dapi, mito-tracker, draq5, er-red, rox-red. also eyfp/tubulin, eyfy/mito, eyfp/golgi, draq5. These dyes aren't cheap and I'm only one i know doing this so I'm checking here.

MitoSOX looks pretty cool. I've never used it myself, but I'm sure you could see some cool mitochondrial dynamics going on. Its a bit pricey though, but all dyes are going to be.

Even at only 8 hours you should probably be able to see a few divisions, which would be cool with hoechst.


Why are HeLa tumors purple? I remember hearing that the tumor where HeLa cells originated from was purple and jelly like, and I've seen pictures from studies with rats and HeLa tumors, and their tumors appear to also be purple. So what makes these tumors purple?

HeLa cells themselves are not pigmented, and usually appear translucent/gray under light microscopy. The growth medium may however be colored, and a common color is magenta.

The tumors themselves will appear purple, as most tumors do, due to the broken vascularization. Tumors commonly secrete growth factors leading to angiogenesis, but the resulting vessel networks are convoluted and not well organized, commonly full of anastomoses. The resulting poor vascularization leads to significant hypoxia, which results in a bluish coloring of the blood.


Is there an 'opposite' neurotransmitter to dopamine? Dopamine is a neurotransmitter  (i.e. chemical) in the brain that gives us great feeling. From here:

Dopamine plays a role in how we feel pleasure. It's a big part of our unique human ability to think and plan. It helps us strive, focus, and find things interesting.

Is there any chemical(s) released in the brain that have an opposite effect to dopamine, that is, some chemical that makes us feel bad?

The release of dopamine has a positive effect on the reward center in the nucleus accumbens. The neuron that releases the dopamine can be inhibited by other neurons, so there gets less dopamine released.
The response elicited by a neurotransmitter, either excitatory or inhibitory, is determined by its receptor on the postsynaptic cell. ~https://www.ncbi.nlm.nih.gov/books/NBK21607/def-item/A7678/


What wasp like insect breeds in clay pots with dead spiders? I found several small clay pots of oval/cigar shape roughly 2cm long in a rarely used window in the house, because a wasp like insect was flying into a small cavity of the window.

I removed one and found dead spiders inside.

I let the rest of the nest alone and closed the window again. I guess I don't have to bother them if they aren't bothering me.

I'm wondering what type of insect is that building such nests? It looked like a cross between a wasp and a hornet.
As far as I know, wasps and hornets build their nests from wood, which gives them a paper like material. This one however is made from soil/dirt.

I'm also not sure if spiders are the only food. But given the street lamps outside, I suspect that spiders are very available and easy to catch.

The region is central Europe.

It's some sort of potter wasp/mason wasp (Eumeninae). The spiders are paralyzed and brought there as food for its larvae.
Here is an example of an opened nest I found on Bugguide.net that looks similar to yours:

I don't know if it's possible to say what species it is from the nest.


Im trying to find out what type of snail this is The snail is pretty large and located in texas.

I'm guessing it's an invasive apple snail, popular in fish tanks.

http://texasinvasives.org/animal_database/detail.php?symbol=15

https://www.youtube.com/watch?v=Pi2wcFPPJsI

Some people keep apple snails as pets, they are very interesting to keep for a while.

Your photo doesn't give enough info, location, sea or pond, clear image of shell, underside, soft body, to say for certain. apple snails have a wide variety of colors.


What are the chances that Tyrannosaurus Rex could roar? Tyrannosaurus Rex is now thought to have possibly had lips. Less of chance of it roar though I was told by a friend just because there are birds doesn’t mean they can’t.

Evolution isn't linear, just because one branch of a tree could/couldn't do something, doesn't mean 70+ million years later descendants could/couldn't do it too?

Careful now: T Rex was not a bird, it was a non-avian theropod. Birds are dinosaurs but not all dinosaurs are birds. In the same way, tigers are cats but not all cats are tigers.

The argument that T Rex could not roar is not only based on none of its closest relatives being able to as you seem to indicate. Dinosaurs (and by extension birds) are archosaurs, a clade that includes crocodilians too and crocodilians are quite a bit more close to the basal form of archosaurs than T Rex was. Crocodilians can only sort of "hiss", not roar in the colloquial sense. And birds cannot roar. This is a decent start to a thought process but this isn't really the argument for why dinosaurs likely didn't roar in the past.

Researchers who have studied the potential vocalizations of prehistoric, non-avian dinosaurs have found indications that similar closed-mouth vocalization to those found in other living archosaurs are very probable: https://news.utexas.edu/2016/07/11/dinosaurs-may-have-cooed-like-doves

Closed-mouth vocalization is not really compatible with what people typically think of as roaring. It still allows a variety of sounds that don't necessarily (though perhaps probably) somewhat resembled crocodialian or simple bird vocalizations. So no, it's not impossible that some non-avian dinosaurs could roar but the current state of our knowledge is that they very likely could not.


Why is Turner syndrome a problem? Turner syndrome is a chromosomal disorder where one of the X chromosomes is missing. For more details visit the Wikipedia page

I don't understand why missing one X chromosome would be harmful. In normal females one of the two X chromosomes is inactivated at an early embryonic stage to a Barr body. For more details visit the Wikipedia page on this.

This X chromosome inactivation can be beneficial. For example, women are less prone to sex-linked genetic disorders due to this X chromosome inactivation.

My questions are:

If only one copy of an X chromosome is active in normal human females, why would having only one copy of an X chromosome cause a disorder?
What does it mean to deactivate parts of a chromosome
Why would it be essential to have two copies of a gene, as only the dominant one is expressed?

Short answer
Some genes on the X chromosome escape X-inactivation. Two copies of these genes are needed for normal development. These genes are also present on the Y chromosome. Hence, healthy males and females both have two copies of these genes. In Turner's, the SHOX gene seems to be one of the culprits, which is needed for normal skeletal development.

Background
It appears that both of the X chromosomes are needed for normal development in females, as some genes on the X chromosome escape X-inactivation. Many of these genes are located at the ends of each arm of the X chromosome in areas known as the pseudoautosomal regions. Although many genes are unique to the X chromosome, genes in the pseudoautosomal regions are present on both sex chromosomes. As a result, men and women each have two functional copies of these genes. Many of these genes are essential for normal development (source: Genetics Home Reference).

Which genes on the X chromosome are responsible is not yet known, but a gene called SHOX seems to be involved, which is important for bone development and growth. The loss of one copy of this gene likely causes short stature and skeletal abnormalities in women with Turner syndrome (source: NIH), see Fig. 1.

SHOX is a transcription factor of the homeobox family. It acts during early embryonic development to control the formation of the development of the skeleton. It plays an important role in the growth and maturation of bones in the arms and legs source: NIH).

Fig. 1. Some developmental malformations seen in Turner's syndrome. source: University of Chicago

FYI - I wrote an answer before checking for duplicates. I think my answer does add additional information (the SHOX gene is not mentioned in the linked question's answer


Why should evolution not be equated with progress? My science textbook says this:

  Evolution should not be equated with progress. In fact, there is no real 'progress' in the idea of evolution. Evolution is simply the generation of diversity and the shaping of the diversity by environmental factors. The only progressive trend in evolution seems to be that more and more complex body designs have emerged over time. However, again it is not as if older designs are inefficient! So many of the older and simpler designs still survive [..] In other words, human beings are not the pinnacle of evolution, but simply yet another species in the teeming spectrum of life.

I am not sure if I agree with this; after all, humans do seem to be more advanced than dogs. Many people have asked me why I thought this was true, so here is my answer: Today, humans could wipe out dogs from Earth if they wanted, but you can hardly imagine  a scenario in which dogs would do the same to humans.

What am I missing here?

I'm glad you've asked the question as it is a common layman misunderstanding.

Dog vs Human

Your example comparing humans and dogs is actually very central to the logical flaw that yields many to equate evolution with progress.

There are several issues when you say

  humans do seem to be more advanced than dogs

Humans are not more evolved than dogs

Humans, dogs, jellyfish, oak tree, fungi, bacteria, .... we have all evolved during about 3.5 billion years. None of the extant lineages is more evolved than any other at least in terms of the number of years of evolution. Note, however, that what matters most when considering evolutionary time is the number of generations. Humans having a rather long generation time, it tends to make fewer generations. In this regard, one could expect a dog to have been through more generations than humans and could eventually be called more evolved but even there it is not that easy. See also Are we “more evolved” than present-day bacteria?

You are a human, be aware of your biases

As @Jamesqf rightly said in the comments, you did not feel like considering the dog's extraordinary sense of smell, better hearing, higher jumps, stronger jaws or protective fur. Not to mention, dogs can typically raise way more offsprings than humans can. Not to become personal but my 8 months old, 9 kg Cocker Spaniel runs 300 meters at the same time Usain Bolt runs 200 meters! You seem to have only considered things that make you human such as opposable thumbs and high cognitive abilities. Coming to cognitive abilities you will note that a puppy learns by association faster than a baby human. Dogs just plateau much quicker than humans.
Make sure that you understand that high cognitive abilities are not a goal or a direction of evolution. While it is hard to measure the evolution of intelligence for both a question of definition and question of measurement tools, it is very very likely that many lineages (incl. eventually the Homo lineage) have evolved toward reducing intelligence at some point (see this post).
You say humans could wipe out dogs from Earth however again it feels very human (and awkwardly combative and hostile) to consider the ability to kill as a measure of progress.

The illusion of considering two variables

You consider a correlation between two variables 1) how evolved a lineage is and 2) how advanced a lineage is. (As discussed in the first point, there is actually no variance in how evolved lineages are if we consider evolutionary time). You are determining those that are more evolved by how "advanced" you visualize the lineage. Your explanatory and response variables are therefore the same and you do not explain anything by saying 'humans are both more advanced and more evolved than dogs so evolution should equate progress'

Definition of progress

A big issue in your question is the definition of progress. For example, if you define progress as an increase of mean fitness (the concept of fitness in biology has nothing to do with bodybuilding, see here) over time, then yes evolution is in part to be equated with progress as increase in mean fitness over time is exactly what natural selection is doing (see the so-called Fundamental Theorem of Natural Selection).

Evolution ≠ Natural Selection

So, let's assume we define progress as an increase in mean fitness over time. As stated in the previous section, this is exactly what natural selection is doing. So, instead of saying Evolution should not be equated with progress, one could say Natural selection is to be equated with progress (as a reminder this assumes a very specific definition of progress)

You will note that I replace the term evolution with natural selection. It is often unclear to laymen but these two terms, while related, are different.

Evolution is a change of allele (loosely speaking, an allele is a variant of a gene) frequency over time. There are a number of mechanisms that can cause evolution, one of which is natural selection (which itself is caused by a fitness differential associated with genetic variance). But there is way more to evolution than just natural selection. Genetic drift, mutations, migration and other demographic elements are all important factors causing the evolution of populations.

You should have a look at Understanding Evolution by UC Berkeley. It is a very introductory online course on evolutionary biology that will teach you about the basic forces that cause evolution.


Aerobic vs anaerobic respiration comparison The following graphs compare glucose decomposition in yeasts (in anaerobic vs aerobic conditions respectively)

My question is, why doesn't the first one look like a straight line as the second one does? Don't they actually follow similar processes?

I think the reason as to why glucose concentration is faster in the aerobic case than the anaerobic one, is perfectly explained by Chris. To summarize:-

  The energy requirement of the organism in both the condition remains more or less
  constant. Since aerobic respiration generates more energy per glucose,(38ATP)
  it takes more time for the same concentration of the glucose to be
  depleted, than it takes in the case of anaerobic respiration where
  less energy is released.(2ATP)

The non-linearity in case of anaerobic respiration can probably be explained thus:-
In the aerobic case, glucose is oxidised to water and carbon dioxide, both of which do not influence the respiratory process. The first step of glycolysis, the phosphorylation of glucose has a very negative free energy change, i.e. is practically irreversible. Therefore a dip in glucose concentration will not affect the rate of energy release and therefore the rate of energy released will stay constant resulting in a linear graph. But in the anaerobic case, the final product is un-metabolised ethyl alcohol. The conversion of pyruvic acid formed as a result of glycolysis to ethyl alcohol is not so strongly irreversible(smaller free energy change), and at high product concentrations, becomes considerably reversible. This means that the ethyl alcohol produced will affect the rate of glucose metabolism, and will retard it by negative feedback (Le chatelier's principle). This will lower the speed of glucose utilisation at low concentrations of glucose, i.e. high concentrations of ethyl alcohol. This reduce the value of slope at lower concentrations of glucose in the graph, and hence produces the non-linearity.


Is transplantation of neurons between species possible? Can brain tissue from one species be implanted into the brain of another species? Because the brain is tolerant to the introduction of antigens (it is said to be immuno-privileged), I was wondering whether neurons would be subject to graft rejection?

If neurons from another species survive in their new host, would they create functional connections?

Short answer
Neural xenografts can survive and form functional connections in the host.

Background
Across-species (xenogeneic grafting) grafting of cerebral cortex from a fetal rat to an adult mouse brain and vice versa, have shown that immunocompetent hosts can reject a graft in less than 30 days. Rejection results in destruction of  the graft tissue presumably by macrophages. Immunosuppression can be used to prevent graft rejection (Mason et al., 1986).

A review article on this topic shows that in the absence of immunosuppression, neural xenografts (donors were fetal to adult-aged) in a rat host brain survive in 37% of the cases in case of a mouse donor, 16% in case of a hamster donor, 9% in case of a rabbit rabbit, 7% from a pig donor, and 0% when human donor tissue was used. Hence, species-separation seems to be a determining factor in xenograft rejection. Induction of MHC-I and MHC-II expression in the xenograft mediates graft rejection in the brain. Hence, despite the fact that the brain is immunopriviliged because of the relative low expression levels of MHC class proteins, it is still sufficient to reject grafts (Pakzaban & Isacson, 1994).

Xenografts have been shown to generate functional afferent and efferent axonal connections with the host brain when grafts of the striatum, substantia nigra, hippocampus and retina were homotopically transplanted.

Functional (behavioral) studies have confirmed these physiological studies. Rats with Parkinson's disease could be successfully treated with substantia nigra grafting from mouse, hamster, rabbit, pig and even humans. Similarly, retinal xenografts have resulted in functional pupil responses, hippocampal xenografts have restored learning deficits, and suprachiasmatic nucleus xenografts have been shown to restore circadian rhythms (Pakzaban & Isacson, 1994).

References
- Mason et al., Neurosci (1986); 19(3): 685-94.
- Pakzaban & Isacson, Neurosci (1994); 62(4): 989-1001.


Emergence of novel protein interactions by mutation of amino acids Are there any examples of proteins that, without coming from a recent duplication event, underwent a mutation(s) that caused it to have a novel interaction with a new ligand, substrate, other protein or molecule? By novel I imply that it doesn’t revert to an ancestral interaction or develop an interaction that is already performed by a close relative. I imagine that such mutations would be extremely rare, and that duplication is almost always necessary to have them fixed in a lineage.

The polymorphism in the gene product of the human ABO locus seems
  to provide an example of what the question demands. It does not
  involve a gene duplication or recovery from loss of function; rather it involves changes that cause
  interactions with a different ligand, and the mutations that produce
  these changes have been identified and examined at a molecular level.

I have described the biochemistry of the human blood group system in an answer I gave to a previous question, so the cartoons of the reactions are reproduced from that answer. The diagrams of the molecular interactions and the gene cluster are new.

Human AB polymorphism

The products of the A and B alleles of the human ABO locus are glycosyltransferases:

One of the enzymes recognizes the sugar, galactose (activated by UTP), whereas the other recognizes N-acetylgalactosamine. There is no doubt that they are the products of different alleles of the same gene, even though this is a member of a gene cluster (see below).

The structures of both these enzymes have been determined and the differences of the interaction with their substrates at the active site modelled as shown below:

There are four residues that differ critically between the two enzymes, three of which are shown. Two of these (Met/Leu 266 and Ala/Gly 268) make contact with the UDP-glucosyl substrates. The third (Ser/Gly 235) appears to affect the conformation of the H-antigen co-substrate.

How is a change in function possible without gene duplication?

The poster expresses the opinion (my rewording):

  “I imagine that such mutations would be extremely rare, and that
  duplication is almost always necessary to have them fixed in a
  lineage.”

Why, then, is gene duplication not necessary in this case? The reason is that the enzymes involved are not indispensable: the product is an elaborated branched cell-surface polysaccharide, the function of which can be served by a range of variants. Indeed, the polysaccharide is functional without elaboration, as in the case of blood group ‘O’, where the enzyme is inactive. However, as discussed in my answer to the previous question, there may be a ‘hidden’ function that has driven the evolution of the polymorphism in humans. It has been suggested that the blood cell surface antigens were used by parasites such as the malarial parasite to enter the cells, and that variation provide resistance (albeit temporary, i.e. until the parasite evolved in response).

Footnote: Gene Clusters of Glucosylating enzymes

The question specifically asks for examples that do not come from a recent gene duplication. However I feel it important to mention the gene duplications that have produced such changes in the gene cluster to which the ABO locus belongs. This is to make it clear that the polymorphism is distinct from such examples.

Animals have the ability to vary the sugars on their cells by selecting from a large repertoire of genes with the potential to specify different glycosylating enzymes. An example is the GT6 gene family (glycosyltransferase family 6):

There are about seven members of this family, not all of which are present in every species. A paper by Turcot-Dubois et al. gives a detailed comparison of the genes in human, rat, toad and zebrafish. I just reproduce the gene map for the human cluster in which the four members of the family are indicated by solid triangles:

The enzymes specified by some of these gene have been characterized by X-ray crystallography, e.g. in this paper by Gastinel et al..


What difference do trans and cis configurations of amide groups bring to the polypeptide chain? Hi I was just wondering whether there would be any difference to the structure of the polypeptide chain, or any changes to a proteins characteristics, if it has more amide groups with a cis or trans configuration.

Apparently the trans configuration is more stable, so more amino acids with a trans configuration can be found within a polypeptide chain. Does this pose any significant characteristic to a protein, and if so what is this characteristic?

Apparently the trans configuration is more stable, so more amino acids
  with a trans configuration can be found within a polypeptide chain.
  Does this pose any significant characteristic to a protein, and if so
  what is this characteristic?

As you said, the trans- form is energetically more favourable. However, in proline the cis- form is energetically similar to the trans- form. The cis- structure introduces a kink or bend in the peptide chain which is seen in case of proline (see this section of wikipedia page on proline).


Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information? What exactly does it mean when a plant has a scientific name that specifies a vairety, for example  Nothofagus solandri var. cliffortioides, or when the name includes an "x", as in Populus maximowiczii Henry x trichocarpa, Populus xcanadensis, or "Crataegus x macrocarpa"?

All of these species are in the USDA Plants database (of plants that occur in the US). There are > 6000 occurences of the string " var. " ~500 occurances of " ssp. " and only a handful occurences of " x " in the database,

Does the x indicate that a plant is a hybrid, and are the varied uses indicate a different meaning?
Does the use of " var " mean that the plant is a variety?

Does it mean that each of these species has been cultivated and/or bred by a human?

Does "ssp"  mean that the plant is distinct yet compatible with others in the species?
is there a way to identify a that a plant is cultivated based on its scientific name?

Let me clarify my answer since it is lower quality than people may like.  To answer the question, my friend is a horticulist and has given a more detailed answer.

Subspecies is the most generic, taxonomically-defined term one rank order lower than species. The subspecies (either an individual subspecies, or collective group of subspecies) are defined to be genetically or morphologically distinct among other subspecies belonging to the same species, yet still produce viable offspring from interbreeding. For example, every type of dog is a sub-species of Canis familiaris, and all dogs are capable of breeding with each other. Subspecies, abbreviated Ssp, may refer to an individual subspecies type, or a collective group of related subspecies when a distinct subset is difficult to define or unknown.

There are a variety of terms that are analogous to subspecies, when the strict definition does not apply, or a different term has been used historically. For example, a varietal is the botanical term, and refers to a named subspecies. For example, grapes are a family of species, divided into the various subspecies, and a varietal is a specific subspecies that we refer to by a more common or familiar name, such as Riesling, Chardonnay, etc. (Grapes are a slightly different case in which most grapes are produced from hybrids or crosses for reasons of withstanding environmental conditions avoiding insect prey and fungal infections.) Microbiology has yet another distinction, called a strain. Strains are often genetically different, and yet all belong to a species. For example, several E. coli strains exist. In contrast, viruses are also given strain/subspecies names which don't technically fit the ICZN definition of interbreeding. Cultivar is a similar term, also from the field of botany. Cultivar is specifically applied to plants that are grown for some agricultural benefit, and have been bred or altered by humans for some reason.

In short, there is a zoological definition of subspecies set out in ICZN. This definition requires viable interbreeding among subspecies belonging to the same species. The term applies to individuals, or groups, as the context dictates. Analogous terms of subspecies are applied (adapted?) to other realms of biology, such as botany, microbiology and virology, but the definitions are slightly different, but consistent within the branch of biology (eg, viruses can't breed so they don't fit the ICZN definition, but the term applies). Ssp can also be qualitatively used to describe an unknown subset of a species (I've seen this used in microbiology mostly).

Crosses/hybrids are indicated with the "x" in the nomenclature. Since I found this confusing, I'm copying from Wikipedia.

  From a taxonomic perspective, hybrid refers to offspring resulting
  from the interbreeding between two animals or plants of different
  species.

  Hybrids between different subspecies within a species
  (such as between the Bengal tiger and Siberian tiger) are known as
  intra-specific hybrids. Hybrids between different species within the
  same genus (such as between lions and tigers) are sometimes known as
  interspecific hybrids or crosses. Hybrids between different genera
  (such as between sheep and goats) are known as intergeneric hybrids.
  The second type of hybrid consists of crosses between populations,
  breeds or cultivars within a single species. This meaning is often
  used in plant and animal breeding, where hybrids are commonly produced
  and selected because they have desirable characteristics not found or
  inconsistently present in the parent individuals or populations. This
  flow of genetic material between populations or races is often called
  hybridization.

There are some horticultural examples of crosses in which an example of interspecific and intergeneric hybrids, and others, are shown.


Why does the stomach ache if you take a brisk walk after lunch or dinner After eating your lunch or dinner, if you take a brisk walk, most of the time your stomach aches. Why does that happen? What happens with respect to the body metabolism?

The reasons for Exercise-related Transient Abdominal Pain are unknown. The current theories are:

Irritation of the parietal peritoneum, a structure lining the abdominal wall as it rubs against the visceral peritoneum, which lies against it and over the top of the abdominal organs
Strain on the ligaments that suspend the abdominal organs (however somewhat unlikely as it occurs during swimming

It used to be thought that blood was diverted away from the diaphragm during exercise causing pain however that has been found to be incorrect.

See this link: http://www.ausport.gov.au/ais/nutrition/factsheets/hydration/cramps_and_stitch


Neanderthal and Sapiens DNA From WIKI:

Modern humans and Neanderthals share 99.7% of their DNA

and

1–4% of the DNA of living non-African humans are found by the Max
Planck Institute to likely come from Neanderthals, a result confirmed
in 2012, and refined to 1.5–2.1% in 2014

What do they mean? If it is similar for 99.7, how it could be that 1.5%-2% is unique genes from Neanderthals?
The Africans do not have them, so African different from European in 1.5-2% ? But that's not true.

Q. “What do they mean?”
A. Two different things

“…share 99.7% of their DNA” is fairly straightforward.

This means that if you compare, base for base, the total DNA sequences of a group of Neanderthals with a group of humans — doing appropriate statistics — you will find, on average, 99.7% identity.

“1–4% of the DNA of living non-African humans…likely come from Neanderthals” is more nuanced.

This is because that 1–4% (generally thought nearer 2%) that is thought to come from Neanderthals could still be 99.7% identical to the human DNA it is thought to have replaced.
How can that be?
First let us assume that there are no genes unique to either humans or Neanderthals. (This may not be true, but the assumption emphasizes that we are considering the same genes.) Now suppose that after the divergence of Neanderthals and humans from their common ancestor the Neanderthals acquired a mutation that produced a new haplotype for a particular gene that spread to all Neanderthals. The percentage difference in DNA would be small, but the haplotype and hence the gene counts as Neanderthal. If it enters the European human population by interbreeding after emergence from Africa, then that gene is regarded to have come from Neanderthals. So the idea is that this is true for approx. 2% of non-African genes, even though the originating Neanderthal DNA may be 99%+ similar in sequence. Likewise, differences are observed between Africans and non-Africans in these gene haplotypes, even though the DNA sequence otherwise is very similar.
I have not discussed the evidence for this 2% gene haplotype difference here as I recently covered it in an answer to another question, specifically on that topic. (Hence my somewhat late interest in this question when it re-emerged.)


Do all plants photosynthesize with equal efficiency? Just what the title states.

Given identical, necessary and favourable conditions (Probably nutrients, humidity, and light but what I mean is all necessary requirements are fulfilled) - Is photosynthesis equally efficient in terms of the amount of sugar/carbohydrates generated by all plants/trees, or are some plants/trees more adept at it?

My background in biology/botany is high-school, so my list of necessary requirements may be lacking for which I crave your indulgence

If you mean the efficiency at which plants convert light energy to chemical energy (in sugar or other reduced C compounds) then there is definitely variability between plants, both at the species and individual level. The photosynthetic efficiency WP page gives ranges of between 0.1 and 8% of total solar radiation converted to "biomass", but these values are not cited. In their review, (Zhu et al, 2008) state that the maximum maximum efﬁciency with which photosynthesis can convert solar energy into biomass is 3.5% and 4.3% for C3 and C4 plants (both observed for crops), respectively. Biomass is not a measure of energy, but perhaps they mean potential chemical energy in that biomass.

Its a pretty complicated question though. Photosynthesis is a complex process involving many interdependent chemical reactions and physical processes. All species (or even individuals) of plants have different morphology, physiology, and biochemistry that influences overall photosynthetic efficiency. In addition, they each inhabit different ecological niches and climate space. Therefore, all species or individuals would have a slightly unique maximum potential efficiency. Here are a couple other efficiency related concepts to consider:

There are 2 systems in photosynthesis that work in tandem, the light reaction and the dark reaction.  The light reaction uses light energy, pigments like chlorophyll, and a bunch of electron transport chain proteins to generate ATP and NADPH. These 2 molecules then provide the reducing power for use in the dark reaction (the Calvin Cycle). In the dark reaction, the enzyme RuBisCO joins CO2 and RuBP, creating simple reduced carbon chains which are then used to assemble sugars. This is an over-simplification, as both reactions are very complex systems with lots of biochemical machinery, but this is the basic process used to convert light energy to chemical energy. To operate at peak efficiency, the entire process must not be limited by incoming energy (light), substrate supply (CO2, RuBP), or nutrients used to construct all the needed cellular and molecular machinery (N, P, K, and many others). In reality, there are limits that vary from plant to plant, species to species. For example, a species or individual with a very reflective leaf surface converts less of the light reaching the leaf surface to chemical energy, thus lowering the output of ATP and NADPH. This reduces the chemical energy supplied to the dark reaction and limits the amount of carbon fixed by RuBisCO. So the reflective surface of the leaf, which might be advantageous to the plant in other ways, has a large impact on overall photosynthetic efficiency (compared to a less reflective leaf or leaves).

If you want to search for more information, there are a number of terms that plant physiologists and ecologists use when describing a plant's (or communities of plants) photosynthetic efficiency. Each of these is used in different ways and can have many variations in units.

Light use efficiency: The amount of carbon fixed per unit of light incident.
Water use efficiency: The amount of carbon fixed per unit of water transpired
Nutrient use efficiency: The amount of carbon fixed per unit of nutrient concentration (usually in leaves).

reference:

Zhu, Ort, and Long 2008 "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" Current Opinion in Biotechnology.


Why do plant leaves turn yellow? Why do plant leaves turn yellow if they don't get enough water or get too much water? I want to know the process.

I've been searching in Google for an explanation, but none of the sites did.
Please describe the process.

Usually it is termed chlorosis, and comes about from an inability to produce chlorophyll. It can actually be determined by a whole range of things, and not just water shortage or waterlogged soil, including nutrient deficiencies, pathogen infection or unbalanced soil pH.

A lot of these factors relate to an inability of the plant root system to properly take up water. As you probably know, water enters the root system to be carried up into the shoot (through the xylem) mostly driven by transpiration, the water pressure caused by loss of water through the leaves. This water carries with it the soil-derived nutrients the plant needs to synthesise substances that can't be produced by photosynthesis. So if you change the water balance (for example by drying the soil) it becomes difficult for plants to get the nutrients they require to produce chlorophyll.

Usually this is mediated by reduced supplies of magnesium, iron or zinc, but because the precursor to chlorophyll is an amino acid, it can also be caused by shortages of nitrogen. pH comes into play because plants use a delicate balance of acidic ions to mobilise (make available to the roots) the nutrients in the soil, and if the soil pH differs too much this becomes untenable.

So in summary it relates both to shortages of key nutrients or changes in key soil characteristics, and the ability of the plant root system to uptake these key nutrients. It is mediated by these effects leading to an inability to produce enough chlorophyll, which leads to the yellowing leaves that you observe.


how many spores are needed to "infect" a wall? There's cardboard box in my room that used to be in another room that had mold all over the walls and it still smells moldy. This probably means the air in my room is polluted with mold spores.(right?)

If only a few spores stick to my wall could this "infect" the wall?

How many spores are actually needed to start infecting the walls in my room?

I threw that cardboard away, but I still wonder about the remaining spores

Yes, the box likely had many fungal spores attached to it since it smelled “moldy”. This doesn’t mean that your room will definitely be contaminated because spores often wait for ideal conditions to germinate. There are fungal spores in the air we breathe all the time, so if those haven’t already colonized your wall then adding the ones from the box are unlikely to cause any problems.

If you do see spots appear, they can be easily removed with a damp paper towel, generic home cleaner, or diluted bleach.


What is the difference between embryology and developmental biology? The question is quite explanatory in it self, I used to think that both are same but then find somewhere that embryology is a part of developmental biology, can somebody please elucidate?

It's a simple sub-set relationship, embryology is a sub-set of developmental (it's a "specialty"). Embryology is only concerned with the embryo - developmental is a larger group, concerned with developments that may occur in other stages of life. Such as the development of secondary sexual characteristics in humans - a developmental thing, but not embryonic.

These are not purely objective definitions and the dividing lines are not well defined. Labels for various scientific fields are only generally applicable, and they are very flexible. For example, many Chemists also do a lot of physics. Many Biologists do a lot of Chemistry. Many Embryology studies dip into developmental stuff. These divisions are not always clear.

Embryology is a part of Developmental Biology in the same way that Biology is part of "Science" - simple sub-set relationship. If you don't understand sub-sets very clearly, you'll want to study up on that relationship - it's very important in ALL sciences, so you can understand things like "All squirrels are animals, but not all animals are squirells"

This statement would be reasonable - "All Embrology is Developmental Biology, but some Developmental Biology is NOT Embryology"


Are there cases when genus name is equal to the name of a higher taxon? Are there any cases when the name of a genus equal to the name of a higher taxon: family, order, class, etc. in botany and zoology?

I answer for botany: no.

The International Code of Nomenclature for algae, fungi, and plants has strict requirements on names:

Article 16.1 has:

  The name of a taxon above the rank of family is treated as a noun in the plural and is written with an initial capital letter. (...)

Article 18.1 has:

  The name of a family is a plural adjective used as a noun; it is formed from the genitive singular of a name of an included genus by replacing the genitive singular inflection (Latin -ae, -i, -us, -is; transcribed Greek -ou, -os, -es, -as, or -ous, and its equivalent -eos) with the termination -aceae (but see Art. 18.5)

And article 20.1 has instead:

  The name of a genus is a noun in the nominative singular, or a word treated as such, and is written with an initial capital letter.

On later article it is explained how to latinize names, with simpler rules (compared to Latin).  So genus are singular and higher rank are plural.

Additionally, for botanical nomenclature, an name for ranks between family and phylum rank is made usually by concatenating a genus name with some suffixes (which are rank specific, see article 16.3, 18.1). So reading a name, one could derive also the rank.  Just few families still have a old name, but still ending with 'ae' (e.g. Compositae, Cruciferae, etc., Art 18.5).  Now (just since 2011-2012 version) there are more exceptions in code, but for historical reasons and for names outside plants in stricter term.

Note: Some old names are automatically corrected with new rules (see e.g. 18.4), so we should have not equal names.


What is the motivation behind the AAAAGCAUAU GACUAAAAAA of the mRNA SARS-CoV-2 vaccine when encoding its polyadenylated ending? The very end of mRNA is polyadenylated as usual, but the BNT162b2 vaccine ends the following sequence, as denoted in this article:
                                     ****** ****
UAGCAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAGCAUAU GACUAAAAAA AAAAAAAAAA
AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAA

This is 30 A’s, then a “10 nucleotide linker” (GCAUAUGACU), followed by another 70 A’s.
What is the reason for this design choice?

To enhance stability and translation efficiency according to {1}:

The 5′UTR (TEV) [8,21] and 3′ UTR (F-I) of this construct have been shown to enhance stability and translation efficiency, as has the 100-nucleotide poly(A) tail interrupted by a short linker (A30LA70, where L = GCAUAUGACU) [22]

References:

{1}
Stadler, C., Bähr-Mahmud, H., Celik, L. et al. Elimination of large tumors in mice by mRNA-encoded bispecific antibodies. Nat Med 23, 815–817 (2017). https://doi.org/10.1038/nm.4356 https://www.nature.com/articles/nm.4356
{21} Gallie, D.R., Tanguay, R.L. & Leathers, V. Gene 165, 233–238 (1995).
{22} Vallazza B, Petri S, Poleganov MA, Eberle F, Kuhn AN, Sahin U. Recombinant messenger RNA technology and its application in cancer immunotherapy, transcript replacement therapies, pluripotent stem cell induction, and beyond. Wiley Interdiscip Rev RNA. 2015 Sep-Oct;6(5):471-99. doi: 10.1002/wrna.1288. Epub 2015 Jun 9. PMID: 26061157. https://pubmed.ncbi.nlm.nih.gov/26061157/


Which species were first described by Charles Darwin? There are many plants and animals named for the naturalist Charles Darwin, such as Darwin's Frog (Rhinoderma darwinii), but which were named by him? I'm finding it difficult to find such a list.

I don't know if these are his earliest descriptions but Darwin did describe several species of Planaria, such as Planaria vaginuloides, P. oceania, plus a new genus, Diplanaria in 1844.

Darwin, C. R. 1844. Brief descriptions of several terrestrial planariæ, and of some remarkable marine species, with an account of their habits. Annals and Magazine of Natural History 14 (October): 241-251, 1 plate.

Perhaps his best known taxonomic work is on barnacles (Cirripedia). He described several species in his monograph first monograph on the group.

Darwin, C. R. 1851 [=1852]. A monograph of the sub-class Cirripedia, with figures of all the species. The Lepadidæ; or, pedunculated cirripedes.. London: The Ray Society. Volume 1

The first monograph was followed by three other monographs on living and fossil Cirripedia.

I believe that most of his writings after publication of On the Origin of Species focused on expanding his evolutionary ideas rather than on descriptions of new species.

You can read nearly all of Darwin's writings online at http://darwin-online.org.uk. With careful searching you can find all (or nearly all) species descriptions.


Is disease transmisson through milk consumption or meat consumption considered direct or indirect transmission route? From an epidemiological point of view, is consumption of raw milk or meat considered as indirect or direct transmission ? Let's take the example of bovine TB. Is consumption of unpasteurized milk considered as direct or indirect ? IMO since milk is a tissue (liquid tissue but still), it is part of the cow, then how could you go more direct than eating the infected animal ?

Direct transmission is through direct contact with the infected person with no intermediary or vector. The Ebola virus and AIDs virus are examples. Indirect would be malaria spread through mosquitos, plague via rats, etc. The common cold spread through droplets in the air could seem indirect, but because of the proximity required, the CDC website lists it under direct. The CDC will provide reliable information for a lot of questions regarding infectious disease.


What does it mean: carrying the stably integrated gene Reading this study
http://www.nature.com/cr/journal/v23/n10/full/cr2013122a.html

They writing

  Multiple exogenous and endogenous genes can be simultaneously activated
  by CRISPR-on

  We tested single, double and triple activation of a TetO::tdTomato
  transgene and the endogenous SOX2 and IL1RN genes (Figure 3A) in
  HEK293T cells carrying the stably integrated TetO::tdTomato transgene

Could you please help me to understand: They talking about exogenous gene. But saying "carrying the stably integrated". Does that mean that this gene (TetO::tdTomato) is in the cell genome (integrated to genome)? If so, what is the meaning of exogenous here?

Thank you!

According to Merriam Webster, an exogeneous gene is defined as " introduced from or produced outside the organism or system; specifically :  not synthesized within the organism or system—compare endogenous".

I believe they refer to the tetO::tdTomato transgene as an exogeneous, or not originating from the species of study


Is it possible to amplify every single piece of DNA through PCR? Is there a way to perform non-specific PCR amplification for the purpose of amplifying every piece of DNA present?

In short; Theoretically yes.

In practicallity no.

Non-specific PCR require random primers to anneal to a target sequence to initiate replication during PCR. Theoretically this should anneal to every combination of bases and therefore allow the amplification of all DNA (or at least in a fragmented form).

Practically, all the primer combinations will have different primer annealling temperatures due to the differential base composition, making the amplification of fragmentation inconsistent, and in others down-right impossible.


What is the DNA/protein charge ratio? To study DNA-protein interaction, I want to do a DNA retardation test by mixing the protein with DNA and afterwarts loading it on an agarose gel to see if the DNA migrates slower. I've found some articles where they do this and they state that they mix the DNA with protein in an 1:8 charge ratio, but I can't really figure out how to interpret this

Could anyone tell me how to calculate a DNA:protein charge ratio? If 1:8 is stated, how should I interpret this?

This is really sounds like a guideline, a starting place, not necessarily your best protocol.

In practice its hard to be more specific as MS says.  The pH of the buffer will affect the charge of the protein, and to a lesser extent the DNA.

Also the protein may have an ideal pH for binding which you could guess is in the range of 7.0-7.4, but might find that the strongest binding depends on unexpected pH and salt concentrations, or the addition of a small molecule.

The affinity of araC for instance is greatly increased by the presence of arabinose in sufficient concentration.

lac Repressor, in contrast releases itself from DNA in the presence of IPTG or  lactose.


What are the differences and similarities between fimbriae and adhesins in microbes adherence factor? Adherence factors in microbes is to attach to a host cell or to an extracellular matrix.
So what is the difference and similarities between fimbriae and adhesins?

Fimbrae is a catch all term to denote the hairlike projections on many gram-negative and some gram-positive bacteria, but exludes flagella. Adhesins are a subtype of fimbrae that serve as organs of attachment to cells or mucosal surfaces. Another type of fimbrae are pili, functioning in conjugation, the transfer of DNA from one bacterial cell to another  (Koneman, I can't even find the year on this crazy book. Used to be the bible of determinitive bacteriology. So many hours.)


What chemicals can be detected in sweat? This question came to mind after reading this article. The article speaks of inducing sweating to determine, by a roundabout fashion, the amount of salt therein. I'm no medic but I find myself wondering whether sweat may be used directly to measure any other chemicals secreted by the body.

For instance:

If one's kidney/liver were to suffer some malady would the body attempt to discharge some additional waste through one's sweat

What chemicals may be detected by analysing sweat?

Cystic fibrosis diagnosis. Here is a link to a paper describing the use of β-adrenergic sweat secretion as a diagnostic test for cystic fibrosis.

Anti-cancer therapy and its effectiveness. This report seeks to determine the levels of the anti-cancer drug sunitinib and its active metabolite N-desethylsunitinib in sweat.

I'll add others later.

Here's a 2004 study looking at a particularly unpleasant sulfury compound produced by bacteria in contact with sweat. It's interesting that the enantiomer of the malodorous compound had a grapefruit-like smell.

This paper puts forth the idea that sweat, which contains lactate, lactic acid, urea (of course) and amino acids, can be used in forensics.


How diverse are dogs in their traits other than appearance? I've asked this question about dogs not so long ago, and the short answer was - dogs are the most diverse looking species of mammals because they got a small number of genes that have a big impact on appearance.

I would like to ask a follow up question- differences in appearance are easy to notice, and I would like to learn about other traits that might be genetically based.

Are there other major differences between dog breeds, like longevity, cognitive performance, friendliness, etc? Or are all dogs more or less the same in traits other than appearance?

Are there plots of traits like these among different dog breeds that identify outliers?

Dogs are highly diverse in their patterns of copy number variation (variation in the number of copies of different genes). This has been shown to be probably related to the diversity in morphology. It would thus presumably also affect other traits such as those that you list, and it seems to at least have been shown for disease susceptibility. Interestingly, wolves have less copy number variation on average than dogs (citation).


What is the evolutionary advantage of red-green color blindness? Red-green colorblindness seems to make it harder for a hunter-gatherer to see whether a fruit is ripe and thus worth picking.

Is there a reason why selection hasn't completely removed red-green color blindness? Are there circumstances where this trait provides an evolutionary benefit?

Short answer
Color-blind subjects are better at detecting color-camouflaged objects. This may give color blinds an advantage in terms of spotting hidden dangers (predators) or finding camouflaged foods.

Background
There are two types of red-green blindness: protanopia (red-blind) and deuteranopia (green-blind), i.e., these people miss one type of cone, namely the (red L cone or the green M cone).

These conditions should be set apart from the condition where there are mutations in the L cones shifting their sensitivity to the green cone spectrum (deuteranomaly) or vice versa (protanomaly).

Since you are talking color-"blindness", as opposed to reduced sensitivity to red or green, I reckon you are asking about true dichromats, i.e., protanopes and deuteranopes. It's an excellent question as to why 2% of the men have either one condition, given that:

Protanopes are more likely to confuse:-

Black with many shades of red
Dark brown with dark green, dark orange and dark red
Some blues with some reds, purples and dark pinks
Mid-greens with some oranges

Deuteranopes are more likely to confuse:-

Mid-reds with mid-greens
Blue-greens with grey and mid-pinks
Bright greens with yellows
Pale pinks with light grey
Mid-reds with mid-brown
Light blues with lilac

There are reports on the benefits of being red-green color blind under certain specific conditions. For example, Morgan et al. (1992) report that the identification of a target area with a different texture or orientation pattern was performed better by dichromats when the surfaces were painted with irrelevant colors. In other words, when color is simply a distractor and confuses the subject to focus on the task (i.e., texture or orientation discrimination), the lack of red-green color vision can actually be beneficial. This in turn could be interpreted as dichromatic vision being beneficial over trichromatic vision to detect color-camouflaged objects.

Reports on improved foraging of dichromats under low-lighting are debated, but cannot be excluded. The better camouflage-breaking performance of dichromats is, however, an established phenomenon (Cain et al., 2010).

During the Second World War it was suggested that color-deficient observers could often penetrate camouflage that deceived the normal observer. The idea has been a recurrent one, both with respect to military camouflage and with respect to the camouflage of the natural world (reviewed in Morgan et al. (1992)

Outlines, rather than colors, are responsible for pattern recognition. In the military, colorblind snipers and spotters are highly valued for these reasons (source: De Paul University). If you sit back far from your screen, look at the normal full-color picture on the left and compare it to the dichromatic picture on the right; the picture on the right appears at higher contrast in trichromats, but dichromats may not see any difference between the two:

Left: full-color image, right: dichromatic image. source: De Paul University

However, I think the dichromat trait is simply not selected against strongly and this would explain its existence more easily than finding reasons it would be selected for (Morgan et al., 1992).

References
- Cain et al., Biol Lett (2010); 6, 3–38
- Morgan et al., Proc R Soc B (1992); 248: 291-5


Normal TSH Levels in Hyperthyroxinemia When it comes to hyperthyroxinemia, how is it possible for TSH to be normal when there is an elevated thyroxine concentration? What I know so far is that it is caused by a mutation in the Human serum albumin (P02768)that carries normally around 10% of the thyroxine.The mutation apparently makes it have a higher affinity for thyroxine, but how does it allow the TSH levels to remain normal?

Since you're asking about hyperthyroxinemia with normal TSH serum levels, I suppose you're talking about euthyroid hyperthyroxinemia.

In euthyroid hyperthyroxinemia, the serum T4 and T3 concentrations are increased, but the TSH concentration remains normal. Besides that, there are normally no clinical signs.

The cause of that increase, as you explain in your own question, is a mutation in a transporter protein (like TBG), or an increase in their concentrations (which can happen in patients with hepatocarcinoma, for instance).

However, the free T4 concentration remains the same, and that is the important value for the negative feedback mechanism that regulates the concentration of TSH:

  The euthyroid status of subjects with FDH has been
  confirmed by normal TSH response to TRH, normal free T4 concentration
  measured by equilibrium dialysis using appropriate buffer systems, normal T4
  production rate and normal serum sex hormone-binding globulin concentration.

Thus, without an increase in free T4 levels, there will be no drop in the TSH concentration.

Source: Impaired Sensitivity to Thyroid Hormone: Defects of Transport, Metabolism and Action.


Cell cycle arrest and apoptosis Is cell cycle arrest needed for apoptosis to occur? I note that some of the factors that mediate cell cycle arrest induction (e.g. DNA damage) happen to be responsible for initiating apoptosis as well. However can apoptosis occur without first arresting the cell cycle?

Apoptosis can occur without cell cycle already being arrested.  For instance, in the case of extrinsic apoptosis, which could be induced by T lymphocytes, for example, a trimeric receptor such as TNF-R or TRAIL-R's containing a DD can be bound at any time by the death ligand secreted by (TNF, TRAIL) or bound to the immune cell membrane (FasL, TRAIL).
The DD (death domain), independent of where cell cycle is, recruits adaptor proteins with DED domains (ie., FADD), which in turn recruit procaspase 8.  Procaspase 8 is cross-activated (becoming caspase 8) when two of them are recruited, then released.  It then begins activating procaspases 3, which begins the actual work of killing the cell (cutting cytoskeleton => blebbing, etc.), activating CAD.
It bears mentioning, however, that once it's kicked in, cell cycle will inevitably stop, since CAD will start fragmenting the DNA...  It also bears mentioning that caspase 8 also activates the intrinsic pathway via Bid => tBid => Bax => Bak => mitochondrial leakage, cytochrome C activating caspase 9...

Sources:

Sayers, Thomas J. 2011. Targeting the extrinsic apoptosis signaling pathway for cancer therapy. Cancer Immunology, Immunotherapy 60 (8): 1173-80.

Eimon, P. M., E. Kratz, E. Varfolomeev, S. G. Hymowitz, H. Stern, J. Zha, and A. Ashkenazi. 2006. Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. Cell Death and Differentiation 13 (10): 1619-30.


Why does a cell need siRNA? My question is about small non-coding RNAs. miRNA and siRNA are both known for mRNA regulation. miRNA can both transcriptionally inhibit and degrade mRNA by cutting it. For inhibition just a small fragment (seed) of miRNA is complementary to the mRNA while for degradation miRNA and mRNA must reach 100% match.
siRNA is almost the same molecule and its only function is to 100% match mRNA and degrade it.

So if siRNA appears to be just a subtype of miRNA, can we confirm that? Or are there any other differences that make these two molecules different kinds of small non-coding RNAs?

So if siRNA appears to be just a subtype of miRNA, can we confirm
  that? Or are there any other differences that make these two molecules
  different kinds of small non-coding RNAs?

siRNA and miRNA are not identical, but similar. It's not incorrect to consider them similar phenomena in biology, but history places them apart and there exist small differences. Both are processed inside the cell by the enzyme Dicer and incorporated into the RISC complex where their target is degraded ("RNA interference"). However, there are important differences, in case you want to be absolutely correct.

siRNA is typically exogenous (introduced from outside by viruses or by engineering). It typically has 100% complimentary to its target mRNA, because we want to reduce off-target binding. If designed well, they target only the intended target and are checked to be incompatible with any other potential mRNA targets, i.e. are designed to be specific.

miRNA is endogenous (occurs naturally within cells) and is single stranded in vivo. Its complimentary is not always 100% perfect, and often has multiple targets. This is the major difference between the two. It pairs with its target mRNA imperfectly; it simply inhibits translation (protein production from the mRNA). In rare cases where it's a perfect match, it causes the cleavage and destruction of the target mRNA just like siRNA. If I remember correctly, plants miRNAs, in contrast to animal miRNAs, usually have perfect complementarity with their targets. miRNAs are also derived from shorter stemloop RNA products than siRNA.

As you probably know, both are non-coding RNAs and do not enter ribosomes for translation. They have similar effects on gene expression. If you are interested in the very first reports of either kinds of RNA, here goes:

miRNAs discovered in 1993 in worms.

siRNAs discovered in 1999 in plants.

Notice the phrase antisense RNA in both titles. Interesting!

Further reading, in case you are interested.

  Why does a cell need siRNA?

This is a very different question. Why? Probably to fine-tune the expression of its genes. Small RNA species can accumulate, aggregate, and regulate mRNA levels in ways that are probably not possible inside the nucleus at the DNA transcription level. Small RNAs are also understood to be epigenetic and function in the cytoplasm and endoplasmic reticulum!