Can you help me identify this "thing"? I found these "things" by chance on my wild strawberries which I grow in my organic garden. Basically, some strawberries are completely covered with them.

They're transparent, they have dots equally aligned and they don't move. I've tried searching for transparent slugs and worms and also faeces but to no avail.

First, I am no expert on this topic, I am simply synthesizing several different sources of information along with the very good work of others.  Since the "thing" featured in this question has appeared elsewhere, it deserves an answer.

These appear to be eggs of Chironomous midges (wikipedia).  This conclusion is based largely on reading the three-part blog by Tom of askanaturalist.com
Part 1, Part 2, Part 3 which is very thorough.  In the last part of that blog, it is stated "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical." Looking at the pictures here and on the other SO questions (here and here) it appears that the eggs are indeed elongated rather than spherical.  Hence they are apparently Chironomous midge eggs.


Why do dendritic cells have CD4/CD8 on their surface? Why do dendritic cells have CD4 or CD8 antigens on their surface? What is their function without the presence of a T-cell receptor?

There is no direct connection between CD (cluster of differentiation) receptors and T-cell receptor (TCR).

CD-receptors are used to label and distinguish different cells belonging to immune system: macrophages, T- and B-cells etc. Dendtritic cells play a significant role as antigen presenting cells and belong to vertebrate (and human) immune system and thus bear certain CD receptor.

These cells participate in the process of learning a new antigen by the immune system. During the very first phase the antigen is taken up by these cells, cleaved and processed. Depending upon the antigenic properties of the molecule it can be recognized as a valid antigen. In this case dentritic cells participate in the process of antigen presentation, where this new antigen bound to the MHC receptor is expressed on the cell membrane.

TCR is the protein that binds to this complex (MHC + antigen) and as long as this binding takes place the signal about antigen is propagated further to the immune system (leading to formation or augmentation of immune response depending upon the cell type which connects to this complex).


How long does it take a leech to attach? How long does it take a hematophagous leech to attach?

Specifically, how dangerous is drinking water which might be infested with leeches?

Presumably, once the leach enters the stomach, it will be quickly dissolved, so the only danger is that it might attach in the mouth or esophagus. Can this actually happen?

(should I ask this elsewhere?)

Apparently, the leech won't wait for you to swallow it, but it'll attach in your aerodigestive tract as soon as it's in it. This case study of children who drank leech-infested water explains pretty well (and in a rather graphical way, in my opinion) what happened to them. I'll copy here just an excerpt (emphasis mine):

  A seven year old girl was brought from a remote village (Kamardin Karaiz) with four days history of cough with blood stained sputum after drinking water from a pond. She also developed pain in her throat and was unable to swallow except for liquids. [...]
  Her coagulation profile was with in normal limits however her hemoglobin level was 9 g/dl. [...]
  On direct laryngoscopy a leech was found attached to the right pyriform fossa with its one end in the glottis which was removed immediately. The patient made a smooth postoperative recovery. On recovery the patient had no dyspnea, stridor or dysphagia and was discharged the next day on oral antibiotics.

This article also reports a historical case of a leech attached into the throat of a Pashtun man in India. The leech was removed with no consequences.

In short, leech ingestion will probably result in having a leech sucking your blood from inside your throat. Although removing it will probably grant a full recovery, it doesn't seem a pleasant experience.


How can paternal chromosomes be present in an egg cell during meiosis I or crossing over, if fertilisation has not yet occurred? I am very confused about crossing over. It is said that crossing over increases genetic variation as it is a combination of paternal and maternal chromosomes. However, crossing over occurs in meiosis 1 but meiosis 1 occurs before fertilisation, so my question is how are there paternal chromosomes in an egg cell prior to fertilisation.

when they say paternal chromosome, they mean chromosome of the father of the organism. Not the father of the offspring of the specific organism. During meiosis ,in order to form the gametes, the chromosomes of the mother and the father of a specific organism interact, because homologous chromosome pairs consists of a pair of the organism's fathers chromosomes, and the mother's.
please tell if you still don't get it.


What is a neuronal loop? Stanford Medicine's OCD page says that

  Many investigators have contributed to the hypothesis that OCD involves dysfunction in a neuronal loop running from the orbital frontal cortex to the cingulate gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to the frontal cortex.

What is a neuronal loop? I have looked it up on DuckDuckGo with no usable results.

The answer is right in the second half of the sentence:

  running from the orbital frontal cortex to the cingulate gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to the frontal cortex

Orbital frontal cortex, cingulate gyrus, striatum, globus pallidus, thalamus, and back to (orbital) frontal cortex: these are all different brain regions. If A connects to B, B connects to C, C connects to D, D connects to E, and E connects back to A, you've made a loop.

The page is saying that there is a hypothesis that there is dysfunction somewhere along this loop in OCD; it doesn't say where exactly, but you can infer that changing something along this path would affect all of the other regions connected in the loop in some way, because they are all causally related to one another.


Blood pH at Higher Altitudes My Campbell's Biology Textbook says the following:

  "For example, when an elk or other mammal moves up into the mountains from sea level, physiological changes that occur over several days facilitate activity at the higher elevations. The lower oxygen concentration in the air stimulates the animal to breathe more rapidly and deeply. It therefore loses more CO2 through exhalation, raising blood pH above its set point.

I was wondering if anyone could explain why blood pH increases as your altitude increases? I know that an increase in pH is a sign of less H+ ions in the blood, but what exactly causes you to lose the ions when you're exhaling CO2?

Thanks!

The following chemical equation explains why pH decreases with increased $CO_2$:

$CO_2 + H_2O \rightleftharpoons   H^+ + HCO^{-3}$

pH changes are the reason why oxygen binds to hemoglobin in you lungs and then dissociates from hemoglobin at other parts in your body where the oxygen is low because cellular respiration turned the oxygen into carbon dioxide. The binding of oxygen to hemoglobin is in turn explained by the Bohr effect.


Can mitochondria with "depleted" mtDNA reproduce? Background

There's a popular group of antibiotics known as fluoroquinolones, abbreviated FQs. They're quinolone abx with a fluorine atom added at position 6 to increase cell permeability. Popular varieties of these drugs include ciprofloxacin, levofloxacin, norfloxacin, and many others. They also go by brand names Cipro, Levaquin, etc. They have a well known side effect of wreaking havoc on the body's mitochondria through numerous pathways.

This stunning image shows the in-vitro result of administering a clinically relevant dose of ciprofloxacin to human tissue for 24 hours (1). The study notes "short, swollen, fragmented mitochondria (smaller aspect ratio) with highly reduced branching (smaller form factor)"

Because the fluorine atom allows for deep tissue penetration, FQs can cross the double membrane of mitochondria, and because FQs are designed to target "double helix" DNA of some bacteria, they also appear capable of targeting the same double helix DNA structure in mitochondria. In bacteria, the FQs bind to the DNA-gyrase, causing breaks in the DNA that are fatal (2) to the bacteria.

Question

A study published in Molecular Pharmacology (3) shows that mtDNA is "depleted" by Cipro:

  Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks. These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase II-like activity, resulting in a loss of mtDNA.

The full text of this study is not available as far as I can tell. I can find scientific literature on depletion of mtDNA (4) but what does this mean for the long term health of the mitochondria / cell?

Can mitochondria with "depleted" mtDNA reproduce, passing on the damage from breaks in the DNA? Or is the mitochondria and cell doomed?
More open ended: Is there any literature suggesting mitochondria damaged by oxidative stress can recover (first image), or are they also doomed?

References

Bactericidal Antibiotics Induce Mitochondrial Dysfunction and
Oxidative Damage in Mammalian
Cells
Fluoroquinolones: Mechanisms of Action and
Resistance
Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells
Mitochondrial DNA metabolism targeting drugs

Can mitochondria with "depleted" mtDNA reproduce ?

If by depleted, you means reduced number of mtDNA copies, then yes, as long some copies still remain, these can be replicated.

Mitochondrial genome is replicated asynchroneously from nuclear genome [Bogenhagen, 1977], through a particular process (review [Holt, 2012]), and is present in multiple copies. These copies can be different, due to mutation.

Mitochondria do not "reproduce" in the common sense, as they do not undergo mitosis, but have a fission and fusion mechanism (review [van der Bliek, 2013]). The fission products get their half of the mtDNA copies at random when the two mitochondria separate.

Mitochondria with depleted mtDNA can (and do, according to your image) undergo fission.

  passing on the damage from breaks in the DNA?

There are DNA repair mechanisms for the mitochondrial genome. In this case, the mechanism of choice to repair double strand break is  microhomology-mediated end joining (MMEJ) [Tadi, 2016], that try to align the ends of the DSB through use of 5-25 bp homologuous sequence. This ususally results in the deletion of some material near the break.

The resulting mutation is conserved, and passed on through replication of this particular mtDNA instance. The mitochondria will contain a mix of mutated and non-mutated mtDNA from now on.

  Or is the mitochondria and cell doomed?

One could say a particular mitochondria is "doomed" if there is no [viable] copy of mtDNA; if it is not able to maintain adequate internal membrane potential, it will try to fuse with other working mitochondria, or be eliminated through autophagy/mitophagy.

The cell itself could be "doomed" if there are not enough mitochondria left to meet energetic demands. (or, through mitochondria-induced aptotosis). Some particular human cell type have hypersensibility to fluroquinolones (tenocyte, chondrocyte, osteocyte), with increased cell death, but other types have not manifested this behaviour. [Barnhill, 2012] The reason for this sensibility/resistance is not elucidated.


Motifs in undirected networks I have an undirected network and I am currently analyzing both three and 4 node motifs in the network. However, I can't find any articles which describe the biological significance of 3 of 4 node motifs in my network. Comparing with randomly generated networks, I am able to deduce that the number of three node motifs and 4 node motifs are significantly higher. However, I am unable to infer any biological significance for this finding.

I am not 100% sure that I understand the question, but I am going to try to answer, based on the following assumptions:

The "number of 3 and 4 node motifs" is not very clear. If I understand correctly, it should be a quantity determined in large part by the degree distribution. You could rewire your network to lose all information about the TRN other than degree distribution and this number is probably very similar (or it is a quite weird network, which would make me suspicious of the data).
Therefore, the number of such motifs of size $k$ is not particularly interesting biologically, specifically due to technical issues such as incomplete ascertainment of edges, etc. The true network may have many more edges, and this will change this number, so the degree distribution is not itself interesting- it is in fact the thing you want to control for.
Therefore, when you compare with randomly generated networks and find different numbers of motifs of $k$ nodes, I suspect the random networks were generated with a different degree distribution. (It is pretty easy to generate networks of the same degree distribution, using e.g. the rewire() function in igraph)
Therefore, I interpret the question to be more specifically: "Among all 3 and 4 node motifs, a subset are overrepresented in my TRN compared to randomized graphs of the same degree distribution. What are some ways to interpret these motifs?" This is the kind of question that is traditionally asked with TRNs in my experience.

As an example of how other groups have analyzed TRN motifs, I suggest looking at Figures 5 and 6 of this paper. For instance, the "feed-forward" motif is overrepresented for links involving some TFs. I believe that it is standard to compare motif distributions to other biological networks, such as the C. elegans neural network. There are references in the Cell paper that could probably help you out further. The wikipedia article on network motifs also looks to have some information, and there are other resources on the internet if you google.

While there is not necessarily a strict biological interpretation of such motifs, they nonetheless can be informative in identifying specific patterns peculiar to different TFs or master regulators.

Caveat
It is possible that I have misunderstood the question or made bad assumptions- my graph theory is superficial. But if I am wrong and you are actually interested in the simple number of motifs of size $k$, that observation is of interest as a "I have a weird graph" theoretical problem, not as a "this is biologically interesting" problem. As a biologist I would care much more about which specific motifs of size $k$ you have, rather than the summed count of all motifs of size $k$.

On the other hand, forgetting about motifs for a moment, a "weird" network could be quite topologically interesting biologically. For instance, do your different clustered components associate with different pieces of biology, like sugar metabolism vs. morphogenesis? That would be expected, but it has very little to do with motifs- they may just be a side effect of that functional topology. In that case, it would be not only degree distribution but also that topology that you would have to control for to make interesting statements about motifs.

good luck!


Inheritance percentiles I am aware that the average DNA contribution from each grandparent is 25%, while the possible range is 0%-50%.  I found a source citing 18%-32% as the "normal" range but this was undefined.  I assume it must be referring to a percentile based on the distribution in a Gaussian curve.

After searching in vain for a chart showing "normal" ranges for each level of consanguinity (sibling, grandparent/aunt, great-grandparent/cousin etc.), I started doing the calculations myself on an Excel spreadsheet... and soon went back to searching.  Surely this information is available somewhere, and there must be generally accepted norms.  The math formulas are well established.

Where should I look to find the results summarized in a compact format?

I want to first know, essentially, the statistical results of flipping 23 identical immutable coins to represent the various generational probabilities.  The facts that the chromosomes are not identical, and that recombination is more likely at certain loci on certain chromosomes, are to be considered later as adjustments to the non-biological math.

I will pursue a statistical answer elsewhere if I can get the "biological" answer as to what percentile is accepted as the "normal" range.  (The 25% average for grandparents has a vanishingly small probability of actually occurring, as it would require enough recombination to equal an inheritance of 11.5 chromosomes from each grandparent.)

Setting up the binomial distribution:
For generation F1 each parent (F0) has a 50% chance of contribution the chromosome (under your simplified model), i.e. p=0.5, n=46 for the binomial distribution. I assume that when you say the 'normal' range you are looking for the mean +- 1 standard deviation? For p=0.5, n=46: mean=23 with standard deviation=3.39116 which helps define: Pr(20≤X≤26)=0.698. So in about 70% of cases a child will inherit 20-26 of their chromosomes from one parent.
For generation F2 each grandparent has a 25% probability of contributing a chromosome so we use p=0.25, n=46 which gives: mean = 11.5, standard deviation=2.93684 Pr(9≤X≤14)=0.6936. So in about 70% of cases a grandparent will have contributed 9-14 chromosomes.


How do I tell if the mosquitos in my New York City apartment can carry Zika? The species that carries Zika, A. aegypti, is unlikely to be found in New York. However, the related species A. albopictus is prevalent and quite concerning. So this question is focusing on A. albopictus (if I may editorialize I would suggest leaving the title closer to the real question of interest, and disambiguating the species as the first step in resolving it).

According to the CDC

  Zika virus is transmitted to people primarily through the bite of an infected Aedes species mosquito (A. aegypti and A. albopictus).

I understand New York has IIRC the aegypti species and Zika has appeared.

My apartment gets mosquitos rather randomly every couple months. Understandably I want to figure out how much effort I should put into preventing or getting rid of them. I can describe their behavior here and maybe that's enough information. If not, do I need to get out a magnifying glass or sequence DNA? (Which I did once in college but I wasn't very good at it).

Their behavior:

I get "bursts" of them at random times in the year - more in the warm months but also in November. We had a warm winter but this still surprised me.
They seem to bite me at night but I've never had a mosquito bite on me. I've had mosquito bites from being bitten by mosquitos before, so unless I've developed a resistance to that in the last few years, that's strange.
I haven't found any evidence of standing water nearby. They don't hover around my sinks or toilets. I read once the Zika carrying strain is on the hardy side and can live off of moisture in walls so this is troubling.

If you're curious my preferred life hack is keeping my living room slightly warmer than my bedroom. And also, you know, killing all of them.

So, are these behavior traits useful? Can I identify them as opposed to other New York inhabiting mosquitos? Is a DNA test necessary?

This is a reasonable question, and I was surprised to find that official information on whether Aedes aegypti is present in NYC isn't very clear. I personally would have thought that NYC was quite far beyond the range of Aedes aegypti (the 'yellow fever mosquito', believed to be the main vector of Zika virus in the ongoing emergence event in South America), and the New York City Department of Health apparently agrees with me:

  Aedes aegypti has not been found in New York City.

...(emphasis theirs) which seems pretty clear cut. However, the CDC recently published a map claiming that NYC is within the potential range of Aedes aegypti.

It's not really clear exactly what they mean by this. From the webpage:

  The new estimated range maps have been updated from a variety of published and unpublished sources.
  These maps show CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States.
  These maps include areas where mosquitoes are or have been previously found.

A related species, Aedes albopictus, is sometimes found in NYC during the summer and is probably capable of transmitting the strain of zika virus currently circulating in the Americas (see for example this recently-published experimental infection study). Aedes albopictus has been the major vector in some previous zika outbreaks in other parts of the world.

(Edit (14th June): A group of mostly-CDC entomologists just published a map of locations where Aedes aegypti and Aedes albopictus have actually been collected between 1995 and 2016 here, and there's an NPR article explaining why the maps are different here).

Whether the density of this species or the temperatures are sufficient to sustain transmission for any length of time in a climate like that of NYC is a more complicated story. The CDC even adds:

  Maps are not meant to represent risk for spread of disease.

But you've asked whether the mosquitoes in question can carry zika, not whether they're likely to be good at it, so I'll leave it there. The short answer is that if they're Aedes mosquitoes, then they might be able to.

So how do you know if they're Aedes mosquitoes? Aedes are visually quite distinctive; they have black bodies with white stripy abdomen and legs:

(Image taken by Muhammad Mahdi Karim; details and license here).

Aedes are also generally day-biters, so if you're getting bitten at night that makes me suspect you've got something like Culex mosquitoes instead (which might be able to spread West Nile virus, although that's a different story). These are dull brown.

If you do find you have Aedes and you'd like to try to identify them to species level, you could collect some dead ones and look at their thorax. If you take some photos and post them here as a species-id question you'll probably get an answer pretty quickly, but this figure illustrates the difference between aegypti and albopictus:

(Image from WHO (1995) Guidelines for Dengue Surveillance and Mosquito Control, Second Edition)

There are better images here but I think these are under copyright.


Is the Basic Reproduction Number in epidemiology dependent on population size? I am assuming that the basic reproduction number $R_0$ of a disease depends on the population size (or the number of susceptible individuals). When $R_0$ is reported it seems to be without such information. Is there a standard population size for reporting $R_0$?

From what I understand (as an ecologist/population modeller), $R_0$ in epidemiology is not dependent on host population size per se, at least not in its basic form. It is also not dependent on the number of susceptible individuals, since it is defined as the number of secondary infections in a fully susceptible population, see e.g. this section in Farrington et al (2001):

  The basic reproduction number of an infectious agent in a given population is the average number of secondary infections which one typical infected individual would generate if the population were completely susceptible.

This is also consistent with the Wikipedia description ("...in an otherwise uninfected population"). $R_0$ is however dependent on the environment (dispersal routes, host-host interactions etc), which also why it is used to evaluate and compare the effect of control measures. Host-host interactions is also dependent on population density, so $R_0$ is indirectly influenced by host population density, and this is partially why estimated $R_0$ values for the same disease will differ between countries and populations.

Fundamentally and conceptually, $R_0$ is the same thing as the Net reproductive rate (often also labelled $R_0$) in demography and population modelling, and it was originally borrowed from demography to epidemiology. As such, the net reproductive rate is often used in for instance pest control to evaluate the potential impact of pest species on agricultural crops, in direct analog to the basic reproduction number in epidemiology (see Emiljanowicz et al, 2014 for a randomly picked, recent example). Most commonly, $R_0$ (both in population dynamics and epidemiology) is calculated from static demographic rates, but nothing prevents you from considering stochastic effects, density dependence or e.g. ways that demographic rates are functions of host density or population size. This could lead to formulations where $R_0$ is an explicit function of host population  density, but that is not the standard use of $R_0$.

To me, it seems like you are asking for the effective reproduction number ($R(t)$), which can be defined by:

  ...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population."

This section is from a WHO paper on meases (Chiew et al, 2013). So basically, $R(t)$ is the average number of secondary cases per primary case at time $t$ (including the effects of immunity and/or control measures). As you can see, $R(t)$ is a function of time, and it can e.g. be used to describe the temporal dynamics of SIR-type models.


Full name for stem cells So during research, my professor mentioned a type of stem cell, a name that was like 5-6 words long, that can be used to treat diabetes by creating an "artificial organ". That hypothetical organ would then be used to create insulin or treat diabetes using other methods.

However I can not remember that name for my life...

This community may not be able to assist me much, as I am aware of the many types of stem cells. This is all the information I have access to, and I cannot contact my professor until the weekend, so it would be great if I could get some prior knowledge about these stem cells; I just need to know the name.....

Thanks in advance.

Human Embyronic Stem Cells (hESC) can be programmed to differentiate into a number of different types of tissue depending on the signals you give or withhold.

Source: BioTime

The company Viacyte is actually developing a technology based on hESC that can be used to rescue loss of function in type-1 diabetes, just as an example. Their process takes hESC to pancreatic endoderm after about a month. The pancreatic endoderm has the capacity to differentiate into beta cells, ductal cells and so forth. He could have also been talking about human induced pluripotent stem cells (hiPSC). Like embryonic stem cells, these can differentiate into "anything," but are derived differently.


Which organisms have the neuroanatomy Roger Penrose supposes play a role in consciousness? In The Road to Reality, Roger Penrose suggests that certain brain structures might play a role in consciousness

  Most particularly, lattice neuronal microtubules, as originally
  suggested by Stuart Hameroff but perhaps also other structures, like
  synaptic clathrins, whose structure closely resembles the c60
  molecules.

He supposes this would have to do with some sort of quantum coherence:

  ...the scheme would require some kind of large scale quantum coherence,
  acting broadly across considerable regions of the brain having
  features in common with high temperature superconductivity.

In general, which organisms have these structures? Are they common?

Microtubules are a structure in the cytoskeleton, they are rope like polymers that grow to a length of about 25 micrometers (25000 nm), and have an outer-diameter of around 25 nm. For comparison, the mean spacing between atoms is on the order of 0.1  to 0.2 nm; so the micro tubule really is micro: about 200 atoms across. In terms of quantum effects though, this is pretty big but not unreasonable. Researchers commonly use quantum dots to play with quantum effects, and these are typically spheres on the order of 10 to 50 atoms in diameter. Note, that we don't know how to couple 5000 quantum dots in one coherent chain (how many you would need to get the length of a microtubule).

So microtubules are small, but they are common! Microtubules are found in all dividing eukaryotic cells and in most differentiated cell types. In other words, that mosquito you just smacked and that philosophers always give as an example of something non-conscious is full of microtubules. This should raise some red flags, but we don't need to go into more detail of microtubules to discredit Penrose and Hammeroff. However, if you love cell biology, take a look at Desai & Mitchison (1997).

So microtubules are probably a bad basis, but why did Penrose want quantum effects in the brain? In The Emperor's New Mind, Penrose suggests consciousness is non-algorithmic and suggests that a magical quantum computer could do these non-algorithmic tasks. The reason I use 'magical' is because a real quantum computer is Turing-complete, if a classical computer cannon solve a problem then neither can a quantum one (of course, if a classical computer can solve a problem, then quantum one can as well and might be able to do it qualitatively faster). For a nice computer science debunking of this part of Penrose's argument take a look a Scott Aaronson's lecture notes.

Why did Hammeroff want quantum-ness? To avoid dualism in explaining consciousness. However, he has gone so far down the reductionist rabbit-hole that he popped out on the other side. He arrived at the same 'magic' we feared in dualism except now he called it 'quantum mechanics'.

The biggest irony of this approach is that Penrose was inspired in many ways by Schrodinger's beautiful take on life. Although Schrödinger does bring in quantum mechanics (both as a useful reduction and as an analogy) he uses completely different parts of it (he uses the discritization of energy levels, and specially avoids issues of the uncertainty principle and superposition of states that made him famous).  Schrödinger would completely disagree with Penrose and Hameroff::

  [I]f we were organisms so sensitive that a single atom, or even a few atoms, could make a perceptible impression on our senses -- Heaves, what would life be like! To stress one point: an organism of that kind would most certainly not be capable of developing the kind of orderly thought which, after passing through a long sequence of earlier stages, ultimately results in forming, among many other ideas, the idea of an atom.

This response can be made precise through quantum decoherence (Tegmark, 2000) and there is little regard for the physical importance of quantum mechanics in the brain (Litt et al., 2006) although Hammeroff (2007) still defends it.


In microarray normalization, why is the normalization factor this? I am working on analysis of a huge number of microarray files. I was trying to understand the need for normalization in microarray data and was going through this paper by John Quackenbush(2002). In the paper, the author mentions that

  There are a number of reasons why data must be normalized, including
  unequal quantities of starting RNA, differences in labeling or
  detection efficiencies between the fluorescent dyes used, and
  systematic biases in the measured  expression levels

Then he talks about a simple normalization techniques. Assuming that  the total hybridization intensities summed over all elements in the arrays should be the same for each sample, he defines a normalization factor is calculated by
summing the measured intensities in both channels-

where Gi and Ri are the measured intensities for the 'i'th array element (for example, the green and red (or experimental and control) intensities in a two-color microarray assay) and Narray is the total number of elements represented in the microarray.

Then the author says this -

This is the part I don't understand. What is the need to introduce $G_k^{'}$, $R_k^{'}$ and why are they what they are? Most importantly, why is $T_i$ equal to $R_i/G_i$ first and then ($1/N_{total}$)*($R_i/G_i$)?

Any ideas?

$G_k^{'}$ and $R_k^{'}$ are normalized values of $G_k$ and $R_k$.

Take say G as $[1,2,3,4]$ and R as $[100,150,200,400]$ as your values and you want to normalize them. This is scaling one of them onto the other and bringing them on an equal level to compare. So in your case the factor is $85$ units. So a unit of R amounts to $85$ units in G.

So to scale G to R, multiply G by $85$ or you can scale R to the level of G by dividing R by $85$. So the values are either $[85,170,..]$ and $[100,150,200,400]$ or $[1,2,3,4]$ and $[1.17,1.76,..]$ from our example.

I think it should be mentioned as $T^{'} = R_i/(G_i*N_{total})$ as in log ratio from the statement in your question.


How does 2,3 biphosphoglycerate works to release oxygen bound to the hemoglobin? I read on Wikipedia that 2,3 BPG binds with the deoxygenated state of hemoglobin and helps in stabilizing it. It was also written that it helps release remaining oxygen from the hemoglobin. How?

https://en.m.wikipedia.org/wiki/2,3-Bisphosphoglyceric_acid

You've answered your own question. The association/dissociation of oxygen is an equilibrium reaction. If you stabilize one state, you move the equilibrium to that state. 2,3-BPG helps release oxygen from Hb exactly by binding and stabilizing deoxy-Hb.


Is there such substances that body can only send to storage (as fat)? I watched video with statement that there are such part of substance in potato chips which body can't use ("empty calories"), that they surely will be stored as fat.

It was here on 12:23:
https://www.youtube.com/watch?v=-jCd6vIF8Co

Is she talking nonsense ?

An empty calorie is still a calorie.

"Empty calories" was coined to describe foods that only provide calories without significant amounts of other nutrients. The idea is that if you're eating a lot of empty calorie foods, you're eating less food with proper nutrition. The implication is that you will not be getting the vitamins, amino acids and other essential nutrients required to sustain you in a healthy manner.

If you can store it as fat, your body can use it. Where does the fat go when people lose weight? Those calories get "burned" when there aren't enough calories in your current diet to provide energy for your metabolic needs.


Common Metrics of Assessing DNA Sequence Quality What are commonly accepted metrics for assessing DNA sequence quality (platform-specific answers are fine)? I am relatively new to this topic, and I want to either find or code (in Python or C++) algorithms for checking sequencing data quality before getting into analysis.

As mention in the comments Phred scores are the quality scores for most sequencing platforms. This value expresses the probability of a base is being called wrongly. You can find more information here. This values can be found in a fastq file coded by symbols.

For example, a phred score of 30 means that there is a probability of 1 base being wrong every 1,000 (that is 99.9% accuracy). In general values around 30 are considered good enough, but it depends on your analysis whether you want to be more more or less restrictive.

Biopython has some examples on how to plot and filter phred scores. There exits lots of other software to do QA checks, for example this one.

You can also check length and distribution of the reads, duplication levels, etc.

In case you need to trim sequences from Illumina there are several stand-alone software like this that you can use.


Why don't all ants have wings? Since the new queens-to-be have wings, it means that ants either evolved from insects that can fly, or insects that can fly evolved from ants, or that we have a case of parallel evolution (which is unlikely).

Now, what evolutionary benefit is there to not have wings?

Certainly ants evolved from insects that could fly.  All the earliest wasps (ants are specialized wasps) could fly.

Building and maintaining wings is expensive in terms of energy.  That's an obvious evolutionary advantage to not having wings.  So if there's insufficient benefit from having wings then there's selective pressure against having wings.


Where do gut bacteria come from in different organisms We know that some of the bacteria in our gut come from the food we eat and our environment. I want to know if there is evidence of bacteria being transferred from the mother to her fetus or from the mother to the eggs.

I'm currently working with insects that have plastic-eating bacteria in their gut. They are raised in isolated spaces so those bacteria would have to come from the bran they eat or from their mother. I'm a physics student interested in biophysics so my biology knowledge is still a work in progress. Thank you.

For technical information on the subject, perhaps start with "vertical transmission insect symbionts" on google, which will lead to you to a variety of info's. Studies for symbionts of lice, fruit flies, mosquitos, termites, isopods, stinkbugs, butterflies and planthoppers.

Insect Symbiosis Vol 3 page 145 states:

Insects have been shown to use transovarian, egg smearing, and coprophagy, transmission, else entirely from the environment at every generation. There is a list of summaries of different insects that use different methods.

this also has masses of information:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967712/

Samples for large insects are taken with tweezers, small insects can be dunked in alcohol and then microbes are extracted.
Microbia RNA can be checked for evidence if the symbionts come from the parents. You can probably figure out a variety of methods for transmitting your insects symbionts, simply applying the wanted gut bacteria to the substrate of new cultures. I expect it can work in between species. you can try smearing eggs too.


How can fresh cavities form at the margins of sliver amalgam fillings on teeth? Silver amalgam fillings predominantly contain silver a known bactericidal agent and mercury which a known toxin and has bactericidal property. So how is it that the plaque bacteria survive near the filling margins and produce fresh caries?

Amalgam fillings are made from an alloy. The properties of the chemical elements bound into an alloy are different than the properties of those elements in different forms. The fillings do not release any biologically significant form or biologically significant amount of either silver or mercury. They are essentially inert.

Plus silver antibacterial effects are quite modest. The existence of fine cracks and gaps between amalgam and tooth provide wonderful hiding places for bacteria - and that shelter is probably more important to the bacteria than any negative effects of the silver.


Analysis of dynamic connectome data? I have heard about existence of full brain connectome data of some worms or fishes. I have heard about GEVI - genetically engineered voltage indicators - that allow to see voltage data at subcellular level. My question is: are there available the mentioned data in processed form (approriate for simulation, mathematical analysis, modelling) and, possibly, are there available some analysis and modelling of them? I am searching materials for neural code that is used in brains and those data and analysis would be very helpful for me.

I am aware of enormous body of coarse resolution MRI imaging data. But my question specifically targets connectome/neuron/subneuron level full data and their analysis.

C. Elegans is the only species with a fully characterized connectome and I don't believe there's been much electrophysiological work done on them. The GEVIs are still being optimized and have their own share of issues particularly with signal resolution - distinguishing between subthreshold changes in membrane potential vs action potential. See the embedded paper. If anything, it will be awhile before the response properties of the neurons in C. elegans are characterized. However, I'm sure you could try modeling smaller circuits where the connectivity and neural properties of the neurons are known.


Why are we using upper teeth and lower lip on labiodental sounds? I came to wonder this when studying language (as well as other same theme question posted just few ago). For example the word "fantastic" we use upper teeth and lower lip to produce F sound, instead of using lower teeth and upper lip, which would work as well with a small practice.

The alternative articulation, called dentolabial, is more difficult to articulate, so it is very rarely used in human language. However, it apparently is common enough in disordered speech to be allocated an ExtIPA diacritic.

The reason labiodentals are easier: Humans normally have a slight overbite.

When the jaw and lips are in a "neutral" position, the lower lip is close to or touching the upper teeth, so with a small vertical movement of the jaw (together with tensing the lip) one can articulate a labiodental. Articulating a dentolabial requires moving the jaw a fair distance forward, to go around the upper teeth before reaching the upper lip. As Ben pointed out in the comments, front-back jaw movement is unusual, a less "common movement in terms of other vocalisations and eating".

Furthermore, since labial articulations are directly visible to observers, learners are especially likely to imitate others' exact articulation. Thus even though labiodentals and dentolabials sound similar, everyone in the population of speakers uses the same articulation (rather than having both articulations in free variation).

Perhaps dentolabials would instead be more common if most people were like this:


Can white eggs be considered as non-vegetarian? I am basically a vegetarian and I find it very difficult to get an actual biological answer for this question on search engine.

There are couple of links which discuss these argument but can not be acclaimed as a proof as being Egg either a veg or non-veg food item. Below are couple of links which I found depicted this in authors perception:

Egg Non-Veg (a proof)
Egg is veg
Types of vegetarian
If it is veg why products are marked with red dots

Is there any biological proof to consider White Eggs either as vegetarian or non-vegetarian?

Of course eggs are not vegetarian. Eggs are, well, the eggs of chickens (usually). Chickens are animals so their eggs are animal matter as well. Whether or not the egg has been fertilized is completely irrelevant, eggs are chicken just as much as drumsticks are.

The color of the egg has nothing at all to do with it. All eggs are, by definition, animal cells. Basically, the chicken's egg is the equivalent to the human ovum. In both humans and chickens, the female will regularly produce eggs and discard them. In the case of a human woman this is the monthly period. When an egg is not fertilized, it is discarded along with some cells of the wall of the uterus. Similarly, in chickens, the female produces and lays eggs. If an egg has been fertilized, it can grow into a new chicken. If it has not been fertilized, it cannot become a new chicken but is most certainly still an animal cell.

So yes, eggs are most certainly animal, not plant or any other kind of matter. Whether or not you should eat them is up to your own moral guidelines to decide. While they are animal tissue, no animal has been killed to obtain them and no harm comes to the chicken if we harvest them.


Why do slime molds pulsate when growing into their fruiting body? An example can be seen in this Youtube video, where the slime mold pulsates as it engulfs a rock in order to form its fruiting body.

Why does this pulsing happen?

What you have observed is called shuttle streaming. This is how Physarum polycephalum (I assume this is the species of slime mold in the video) and many other slime molds move.
I found this here;

The movement of P. polycephalum is termed shuttle streaming. Shuttle streaming is characterized by the rhythmic back-and-forth flow of the protoplasm; the time interval is approximately two minutes. The forces of the streaming vary for each type of microplasmodium.
The force in amoeboid microplasmodia is generated by contraction and relaxation of a membranous layer probably consisting of actin (type of filament associated with contraction). The filament layer creates a pressure gradient, over which the protoplasm flows within limits of the cell periphery.
The force behind streaming in the dumbbell-shaped microplasmodia is generated by volume changes in both the periphery of the cell and in the invagination system of the cell membrane.


What causes midcycle FSH surge in the menstrual cycle? I have encountered contradictory attributions to the causal factor of midcycle FSH surge. Whereas some sources attribute it to the relatively high estrogen levels (1), others say it is because of increasing amounts of progesterone (2).
I am confused.
(1) http://www2.hsc.wvu.edu/som/physio/classes/pcol260/classroom/notes/reproductive.htm
(2)
https://www.ncbi.nlm.nih.gov/books/NBK279054/#!po=1.17188

The LH surge is began by a impressive rise of estradiol produced by the preovulatory follicle and results in subsequent ovulation.
The LH surge stimulates luteinization of the granulosa cells and stimulates the synthesis of progesterone responsible for the midcycle FSH surge.


What is the water and fat composition of the human brain? Everywhere I look online says the brain is about 60% fat. But when it comes to water, I see numbers like 70-75%. One webpage even makes both those claims back to back! That doesn't make any sense. So what is it, really?

Whenever you see a percentage, you should think "Percentage of what?".  Not doing this is usually at the root of the trouble people get into with percentages.

The water and fat percentages mentioned in the question are certainly not percentages of the same thing.  The sources of the figures should make clear what the percentage is of, but non-scientific writing quite often fails to do this.

In the paper "Lipid composition of the normal human brain", there is a table giving percentages of water and lipids (fats), and at the bottom of the table it says:

  All values, except water, are expressed as a percentage of dry weight.

This is a common approach, as, for example in this table from a textbook the lipid percentages are also given as percent of dry weight. This is convenient because water is such a large part of most organisms, and also dry weight is what is usually measured in the laboratory.

Thus the water percentages you are seeing are presumably percentages of total weight, and the fat percentages are percentage of dry weight.  You can convert the latter to percent of total weight by multiplying by the dry percentage of the brain, which is what is left when you subtract the water percentage from 100%.

Thus, assuming say 73% of total brain weight is water, the 60% fat figure would translate to about 16% of total brain weight is fat.


How does injecting low doses of allergens cure allergies? Allergy shots (aka. allergen immunotherapy) help people adapt to allergens by injecting a gradually increasing doses of one or more allergens.

Does this procedure tell the body that this allergen is safe and there is no need to mount a response to it? In other words, does this mean that there will be no reaction at all rather than just a reduction in the allergic reaction.

But are there ways to tell the body that this allergy is safe and there is no need to amount a response to it?

Yes, that's what allergy shots (Exposure Therapy) does. Exposure Therapy is an effective, albeit sometimes imperfect, method of letting the body know that a substance is common and that it shouldn't mount a response to it. Over time the body re-calibrates itself to accept the allergen, although in some cases it's never fully accepted.

A complete "cure" can be attained via allergy shots, but the extent of the therapy's success will rely almost exclusively on the individual's immune system. Some people can be cured completely, others will never be cured.

  If not, why not?

There will probably not be a general "allergy" cure anytime soon because we're still not 100% sure why the body responds in such an overprotective matter sometimes and not others. Even if we fully understood at some point, there are many ways which the immune system can go awry that result in allergies.

There isn't a single, double, or triple point of failure along the line - just about any immune cell, whether Mast, Eisonophile, T-Cell, T-Reg, B-Cell, etc. can misidentify a substance and contribute to an allergic reaction (although some are more likely candidates than others). More than that, just about any substance can become an allergen for people. There's a well-studied case of a woman who became allergic to Copper because of repeated exposure via an early version of IUD that she had implanted.

So with nearly every immune cell capable of mounting a response, and nearly anything in the world capable of provoking a response, the best route - at least thus far - has been repeated, increasing exposures to teach the body what is "OK" and what isn't. The absolute best way to avoid allergies later in life is to simply promote outdoor playtime and a widely variable diet to children while the immune system is operating at peak efficiency and learning capability.


What is a Slurry in Microbiology? I have been reading this article and they refer to this thing called 'slurries' that can be made from soil samples. This is in the context of being some sort of microbiological method.

"slurries can be made from these soil samples"

Does anyone know what this is? When googling it, I can not find a clear answer to what the method does.

Apparently, microbiologist use this term to describe the process of culturing microorganisms from soil. You make a 'slurry' which has both growth media and the soil (which would fall under the english definition of a slurry) and incubate it waiting for growth. Media(Liquid) + soil = Slurry


What is the name of this plant which is located in Hyderabad city of Telangana State,India? I found this plant in Hyderabad city of Telangana State,India.Many people of Hyderabad city have planted this flowering plant.I don't know the name of this plant.If it's flower treated as a circle,the flower has diameter of nearly 6cm length.Can any one tell me what is the name of this plant?

From the twisted overlapping appearance of the petals it is a member of the Apocynaceae family.  So I searched for "Apocyanaceae india" and found images consistent with your picture.  Good chance it is Allamanda blanchetii or Purple Allamanda.  Here is a picture comparable to yours (source/CC0).

Here's a bit about the plant and Wikipedia has a short page.


Reaction of the body to heat In massage school we are being taught hydrotherapy -- applying cold and heat to specific areas.

It says that when applying cold, first the body goes through vasoconstriction, and then later vasodialation. That makes sense -- preserve heat through the former, but if the cold is applied for too long the body still has to keep the cells alive, thus the latter.

What doesn't make sense is this passage, in relation to applying heat:

  Law of Action and Reaction: Initially blood will rise to the
  surface, applied for too long the blood will recede to the interior
  causing inner congestion to be greater than before

Is that true?

Local warming of a patch of skin will cause vasodilation. However, after prolonged warming there is a 'die away' phenomenon, is which blood vessels slowly constrict back to their normal diameter.

  Johnson JM, Kellogg DL Jr. Local thermal control of the human
  cutaneous circulation. J Appl Physiol (1985). 2010;109(4):1229–1238.
  doi:10.1152/japplphysiol.00407.2010
  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2963328/


Can my eyes adjust instantly to my friend's glasses? My eyesight is pretty much perfect, but I noticed that whenever I try any of my friends glasses, from really thin to extremely thick, my eyes seem to adjust to them within seconds and let me see perfectly fine. Is this weird or abnormal, I was just really curious.

The phenomenon you described as "my eyes seem to adjust" is a particular case of accommodation - adjustment of the dioptric power of the crystalline lens to the object's distance.

When you place a lens before your eye, any object seen through this lens will initially appear at a different distance (and of different size of course) and will be blurred at different degrees (i.e out of focus). Thus, to overcome this discrepancy the eye must accommodate.

Now, the amplitude of accommodation is the maximal power which can be added to the current power of the crystalline lens. The younger the subject, the higher amplitude of accommodation he/she has:

Thus, if one young emmetropic person (person 1) wears some other person's myopic glasses (person 2) with a concave lens with minus power to lessen the actual "overpower" of the optic system, and this power does not have the refractive error of person 1's has (less myopia if they have any "hidden" myopia), the eye must accommodate, i.e. by increasing the convexity of the crystalline lens. If the amplitude of accommodation is much higher than the glasses in question, person 1 will easily adjust to these glasses by elimination of dioptric discrepancy.

Thus, Sherlock Holmes could deduce the following:

You are a young person (under the age of 30) with a high amplitude of accommodation.

You have a lot of "four-eyed" friends suffering from myopia.

From these facts the fiction writer could assume even your nationality (developed country) and level of close work (reading books, using computers) your friends are doing but - let's leave those assumptions to writers! :)


qPCR (weird ntc curve, amplifies before templates and reaches plateau quickly) I'm new to qPCR, and I’ve been testing the AR expression on canine tissues. I’m currently using a pair of primers that have been tested in other article for canines.The issue I’m having is  that I have very early amplification of ntc AR (before the amplification of cDNA templates) but also this amplification curve looks weird since it reaches quickly the plateau phase (flattened). This problem persisted even after changing to a much more specific cycling. If anyone has any tips, or ideas on how I may be able to explain this, I’ll be very gratefull.

The cause of the signal in the no template control will be contamination. It could be that the reason for the different plateau positions is the presence of reaction inhibitors, depletion of reagents, or possibly different binding efficiencies between template (and contaminating DNA) and the primers. I'm not sure about that last one but it kinda makes sense in my head: any contaminating DNA that binds to the primers probably won't bind as efficiently as the template that the primers have been designed for so the reaction is inhibited by accumulation of dsDNA faster.

Either way the cause is going to be excessive contamination. Try using more template in your samples (increasing you signal to "noise" ratio), or be more careful when preparing your samples.

There are extraordinary measures that can be taken to remove contaminating DNA (e.g. treating the water with DNase and then deactivating it) but these often aren't necessary and the added steps can actually increase contamination, it's usually best to keep it simple.


Gene copies vs. gene paralogs - what's the difference? I'm trying to get into the theory and practice of gene copy number variation (CNV) analysis, but there is something basic confusing me, which I couldn't yet figure out. Sorry if this is a dumb/trivial question - would appreciate your help anyway.

My confusion is regarding the terms 'gene copy' and 'paralogs'. As far as I understand, paralogs are created when a gene undergoes duplication (never mind by what molecular mechanism), and then starts accumulating mutations as evolution proceeds. So, if gene X was duplicated to create another X, and then X changed to become X', are X and X' considered copies of the same gene, or are they paralogs? Is it a matter of applying some threshold on the sequence similarity between X and X', so they are considered copies up to the point where they diversify enough? Or maybe gene copies are expected to be perfect duplicates? If so, I'd guess that finding such gene pairs is very rare... Maybe it's a matter of function, so once X' gets a different function from X (neo-functionalization), it is considered a paralog? This is a rather complex and difficult to measure definition...
To make things less theoretical and more practical, lets limit the conversation to the context of whole genome sequencing analysis. Let's say that I am annotating a newly-assembled genome, and let's assume that the assembly is good enough so gene copies are not collapsed, but rather are located in their respective genomic positions. How would you look for gene copies and paralogs, and how do you make the classification?

Could anyone clarify this point for me, or refer me to relevant literature?
 Thanks a lot!

The general term "copies" has multiple meaning with reference to genes. In diploid organisms for example, we have two copies of each gene (except those on the Y chromosome). However, these copies are called alleles. Copies that are due to duplication are called parlalogs. There is no distance criterion for differentiating copies or parlalogs. Once duplicated, there are two copies. But the consequences of paralogy would depend on differences, so the question is interesting. At the first generation after duplication, if both copies included all of the upstream regulatory elements, it would be hard to identify which of the copies was the original, since they would both be identical. But over time, if one were to evolve a new function or (more likely) accumulate frameshift substitutions, the altered one would be called the paralogous copy (relative to comparisons across species).


Why are there no known photosynthetic archaea? I'm taking a microbial physiology course and we noted that, while some archaea are phototrophic, there are no known photosynethetic archaea.  Are there any physiological characteristics that make archaea less suited for photosynthesis?  Or is it simply a matter of there likely being photosynthetic archaea, but they have not yet been found (which seems like it could easily be the case, given that there are many extremophilic archaea)?

There are photosynthetic archaea (such as Halobacterium) but the mechanism is different. They use rhodopsin-like ion pumps (bacteriorhodopsin and halorhodopsin) to move ions against the gradient and produce ATP via chemiosmosis (like mitochondria).


What is the difference between "physical interaction" and "genetic interaction"? I searched sac1 in uniprot to know more about this gene. in interaction I selected this link and there I see that this gene has some "physical interactions" and "genetic interactions". I am wondering that what is the difference between "physical interaction" and "genetic interaction"?

Physical and genetic interactions are described in the help wiki, accessed via the top menu bar on the page you linked to.

Physical interactions refer to experiments where the gene product (protein) has been shown to physically interact with another protein, such as by co-immunoprecipitation, fluorescent staining, yeast two-hybrid system, etc.

Genetic interactions refer to experiments where changes in a certain gene reflect in changes to your gene of interest (or vice-versa) - dosage lethality, dosage rescue, synthetic haploinsufficiency, etc.


What is the name for the opening in the mouth for the nasal passages? Is there a proper anatomical name for the opening in the soft palette where the nasal passages enter the mouth?

From what I understand from your comment is that you are asking for opening which connects the nasopharynx to oropharynx.

This opening is is connecting two parts of pharynx , acting like a bridge therefore it was named as Pharyngeal/Nasopharyngeal isthmus.

According to this site:

  isthmus of pharynx

  Type:Term

  Definitions
  1. passage posterior to the soft palate by which the nasopharynx and oropharynx communicate (i.e., the junction of nasopharynx and oropharynx), closed during swallowing by elevation of the soft palate and contraction of the posterior fascicle of palatopharyngeus (muscle), forming a Passavant cushion.

  Synonyms
  isthmus pharyngis , pharyngeal isthmus

Source of image: Textbook of Anatomy: Head, Neck, and Brain : Vishram Singh


Are there adaptations in tropical fish to compensate for less oxygen in water? Warmer water means that the amount of gases- especially oxygen- dissolved in it reduces, since solubility of gases in a solution in most cases decrease with an increase in temperature.
I'm interested in knowing if tropical fish have any adaptations to account for this reduced oxygen compared to fish in colder waters. Any modification of the gills maybe?
Referencing the below articles, I have come to the conclusion that tropical fish end up migrating to shallower waters or cooler habitats due to the oxygen depletion, showing that this decrease in oxygen is serious enough to affect them. However, this may be due to excessive heating of oceans due to global warming. I'm curious about whether fish in tropical regions have any adaptations for living in ocean water that is heated purely by natural means, not anthropogenic ones.

References:
https://www.usgs.gov/media/images/temperature-affects-dissolved-oxygen-concentrations
https://www.pca.state.mn.us/sites/default/files/wq-iw3-24.pdf
https://www.sciencedaily.com/releases/2015/06/150604162455.htm
https://www.nationalgeographic.com/science/article/150313-oceans-marine-life-climate-change-acidification-oxygen-fish

Fish that live in cold water for most of the year actually have particularly strong hypoxia-tolerance adaptations, i.e. from summer heatwaves and algal blooms, compared to fish that are better oxygenated by waves and flowing rivers.
Goldfish and other fish are able to rapidly change the surface area of their gills in less than a day.
Carp, killifish, goldfish and oscars have 2/3 times as much glycogen in their bodies than river fish i.e. rainbow trout.
There's a lot of research into the biochemistry of fish's oxygen response, i.e. gene expression changes, things like decreased expression of genes involved in the citric acid cycle.
Probably you will find most of the information on the wiki page, there are also summaries of current advances in the field.
On coral reefs, oxygen is a limiting currency for all the fish and zooplankton. The reading suggests to me that hypoxia adaptations depend mostly on heatwave events and low current waters vs rivers and coastal waves than by tropical vs pelagic and temperate regions.


Definition for different arrhythmia I am wondering if there is an organization, a document or a research that standardize all the rhythms? Such as describing how long should the ECG be flatline to be considered as asystole? The rhythm I am focusing on is:

Asystole
Missed beat
Tachycardia
Bradycardia
PAC
PVC
Bigeminy
Trigeminy
Atrial Fibrillation

Basic Cardiac Rhythms – Identification and Response (The University of Toledo, Medical Center)

This quite thorough one-page source describes:

Basic heart anatomy and physiology
The meaning of the waves in ECG
Examples of ECGs for most arrhythmias with timing, causes, symptoms and treatment

Here's Pocket Guide to Neonatal ECG Interpretation (NICU INK Book Publishers) - an one-page source about arrhythmias in infants.


"Enhancers" of enhancers? I am looking for examples (if any) of genomic regions which regulates the activity of enhancers, either augmenting or reducing it. Essentially some kind of enhancers (or repressors) of enhancers to make a Russian doll analogy. I know about epigenetic markings but I am really looking at an example of a DNA region directly acting on a enhancer similar to an enhancer acting directly onto a promoter.

I am asking that because I couldn't find any examples and was wondering if I missed such a report/paper.

If you're looking for a strictly and directly DNA-DNA mediated effect (no histones, no transcription involved) I'd look for sequence effects on chromatin remodelling, modulating access of transcription factors (TFs) to their elements. Something about this might be in this paper:
Szerlong, H. J., & Hansen, J. C. (2011). Nucleosome distribution and linker DNA: connecting nuclear function to dynamic chromatin structure. Biochemistry and Cell Biology = Biochimie et Biologie Cellulaire, 89(1), 24–34. doi:10.1139/O10-139


How to make a fake auditory signal? My question is about making fake auditory signals. The ear collects sounds from the environment, which are transformed into a neural signal by the hair cells in the inner ear. This signal is sent through the auditory nerve to the to brain, where it is decoded into a hearing sensation.

Now can we make fake signals and feed them into the auditory nerve to bring it to the brain? E.g., instead of the ear collecting sound, could we use an electrical instrument for collecting sound and convert this signal into a neural signal in the auditory nerve?

Devices that bypass the hair cells in the inner ear and directly stimulate the auditory nerve are called cochlear implants. Cochlear implants are used to treat deafness caused by the loss of hair cells in the cochlea. The hair cells are the sensory cells that convert sound vibrations into electric neural signals (Purves et al., 2001). With state-of-the-art devices, the better performing implant wearers are able to talk over the phone(!) An exclamation mark is in place, because it means they can understand the spoken word without the need for lip reading or sign language. Hence, cochlear implants are the answer to your question, but they definitely are not designed to generate fake signals. Instead, they are used as an effective treatment for deafness and are capable of transmitting meaningful speech information.

Cochlear prosthetics consist of an array of typically 20-24 electrodes that are inserted in the scala tympani of the cochlea. The inner ear is tonotopically organized, which means that high frequencies are coded in the base of the cochlea, while low frequencies are encoded in the tip. Hence, each electrode stimulates a separate frequency band (Fig. 1). By using a microphone and sending the acoustic signal through a filter bank, a number of auditory frequency bands can be obtained equal to the number of electrodes in the implant. After this speech processing step, the acoustic frequency bands are converted into trains of biphasic pulses. These pulse trains are sent to the electrodes in the cochlea, which then activate the auditory nerve directly, effectively replacing the degenerated hair cells in the inner ear (Stronks, 2010).

Fig. 1. Cochlear implant. Source: Mayo Clinic.

References
- Purves et al., Neuroscience (2001) 2nd ed.
- Stronks (2010). PhD thesis, Utrecht University


Can someone identify this tree in Playa Del Carmen, Quintana Roo, Mexico? I just noticed this tree in Playa del Carmen in Yucatan. It was swarming with bats, the bat seem to be eating either the fruit or the flowers of the tree. Any idea what it is?

The photos are blurred. We need a pic of the bark and of the fruit, sliced. Does it have pips or a nut? Perhaps a Palaquium variety, i.e.  Palaquium Gutta, which is for producing latex/rubber, because it's in a garden and its a useful commodity plant previously grown in south america. Perhaps slice and study the fruit for a better ID.
Latex plants attract bats.
You can check the bark for latex.
https://youtu.be/6DJHD91VKKY


What is this spider spinning a bright green web? Here is the picture of it I took with my phone while I was out working:

Here is a close up:

Location: Texas (winter).

Your image is not the best one, but this is probably the Magnolia green jumper, Lyssomanes viridis.

Here is a better image of it for comparison:

It also matches your location. According to the Wikipedia page linked above,

  the species is native to the Southeastern United States plus Texas, and as far north as Maryland.


A question about microbes growing media I was told in my microbiology course that blood agar can be put in GasPak system (anearobic) to grow strict anaerobes, but why would someone use blood-dependent bacteria in this experiment as these blood-dependent bacteria will be aerobes or at least facultative

You can put any media in a GasPak or other anaerobic system depending the type of anaerobic growth you are looking for. Sometimes blood is simply added to media to meet nutritional requirements of an organism. I use Columbia Blood agar often as a general purpose anaerobic medium. In a collection of 100+ obligate anaerobes I am working with, around half grow well on columbia agar with 5% sheeps blood, and many of those will not grow on Columbia without this blood amendment. As an added bonus, I can easily spot certain common contaminants growing on my plates by their hemolysis paterns.


How to transform snail shells into a fertilizer? I heard that the chemical structure of the snail shell has elements that help in waste water treatment and in some cases as a fertilizer?

What is the process used to render snail shells into fertilizer and how effective is the derived fertilizer compared his regular peers on the market ?

Snail shells are composed largely of calcium, which is often used as fertilizer. As for wastewater treatment, I've heard about shells in general being used, mostly for their absorbent properties. I found this paper, which isn't long & might provide a bit more detail.

Hope that helps!


Number of transcription factor genes in the human genome What is the number of the transcription factor genes present in the human genome? Does this value differ compared to Mus musculus, Drosophila melanogaster, Arabidopsis thaliana, C. elegans and S. cerevisiae? Additionally, does the proportion change between eukaryotes and prokaryotes?

Here I will assume we are talking about eukaryotic sequence specific transcription factors (ssTFs) and try to answer your first and part of the second question. There is in any case not definitive answer yet.

An estimate of ssTFs genes in humans is given in the 2009 Nature Reviews Genetics paper by Vaquerizas, JM et al, A census of human transcription factors: function, expression and evolution.

An excerpt from the abstract:

  Here, we present an analysis of 1,391 manually curated sequence-specific DNA-binding transcription factors, their functions, genomic organization and evolutionary conservation.

The numbers are somewhat higher now. Wingender et al. have counted 1,558 human genes in their TFClass database 2013 NAR paper. In their 2014 NAR paper they included 1,557 human, 1,147 mouse and 1,105 rat orthologs.

Another way to look for this information is to see the number of entries listed in TF databases, like for example JASPAR. This has the advantage of including other species. However, the coverage here depends on the availability of position weight matrices (PWMs) for the binding specificities. Many uncharacterized TFs may not be found.

To try to answer your third question, that is, what is the proportion of TFs in the different species, a naive approach would be to divide the number of predicted TFs by the number of predicted genes in the target genome. For example, taking the latest estimates above with the predicted number of coding genes from Ensembl database (version 78) will return these percentages:

# Human
100 * 1557 / 20364 = 7.64%
# Mouse
100 * 1147 / 22606 = 5.07%
# Rat
100 * 1105 / 22777 = 4.85%

This suggests humans have a slightly higher proportion of TFs than rodents. However, these differences are not too big and may be dependent on the accuracy of the different estimates on TFs and gene numbers. An in itself, these numbers are not so interesting.

A much more interesting question is whether TF families have expanded more or less in different species (that is, whether the number of  proteins within each family has increased, regardless of the proportion to the total number of genes in the genome). I could find at least one paper where this has been done systematically for several eukaryotic species, covering animals, plants and fungi, and focusing on TFs common to the ones found in plants. The main conclusion of the paper is that some TFs families have expanded more in plants than in other organisms. Quoted from the abstract:

  To investigate if differences exist in the expansion patterns of TF gene families between plants and other eukaryotes, we first used Arabidopsis (Arabidopsis thaliana) TFs to identify TF DNA-binding domains. These DNA-binding domains were then used to identify related sequences in 25 other eukaryotic genomes. Interestingly, among 19 families that are shared between animals and plants, more than 14 are larger in plants than in animals. After examining the lineage-specific expansion of TF families in two plants, eight animals, and two fungi, we found that TF families shared among these organisms have undergone much more dramatic expansion in plants than in other eukaryotes. Moreover, this elevated expansion rate of plant TF is not simply due to higher duplication rates of plant genomes but also to a higher degree of expansion compared to other plant genes.


Leaves growing on a leaf of a Begonia I've a Begonia species. Somehow it started to grow new leaves on top and right in the center of an existing leaf which you can see in the center of the image. Why is it doing this? Apparently it is not a disease because the Begonia itself is growing fast. Will the new leaves eventually become a new Begonia which can survive on its own?

The phenomenon you are observing is probably Adventitious buds. The plantlets can develop on intact leaves or on injured one.

Back to Begonia, this phenomenon usually occurs on injured leaves, so, probably, the plant was injured during movement/by insect or by other means and because of this started to create plantlets.


Lab experiment: Enumeration of Leukocytes The images below were obtained in an experiment to enumerate leukocytes in a blood sample using Neubauer counting chamber.

The following solution was prepared and added to the Neubauer chamber and viewed under a compound microscope:

100 microlitres of acetic acid (acidic reagent to haemolyze RBCs) + 50 microlitre of Leishman's stain + 1-2 drops of blood.

Are these granular transparent circular objects in the images the leukocytes? If yes, do these include the smaller ones too? I am unable to decide which ones to take into account.

Moreover is this count normal (for instance, I counted around 250 (excluding the very small ones and applying the margin rule) in the top left box of the grid (Image 3))?

First I'd make sure all the RBC were gone just by visually inspecting. What should remain are your WBC and platelets at this point, and platelets are tiny so you can probably count anything between 5µm and 25µm. So for me that would include basically everything I can see minus background or debris.

So the problem now is with quantifying your count. You should know what the volume of your blood is, and here's why: What you're doing with a hemocytometer is counting #cells in a given volume, but you also diluted your whole blood with 150µL before you counted. So for example if a drop is ~60µL, and you diluted it with 150µL your dilution factor is 3.5, and it's important because your cell density equation is

For reference, you typically end up with 4-10 million leukocytes per mL of blood, however.


properties of lamps for indoor plant growth Ikea has a brand of hydrophonic start kits called vaxer. Part of their offering consists of lamps that aid in the cultivation of the plants (example1, example2 and example3). There are other companies offering lamps that should help plants grow. Here is an example on ali-express.

When I compare the lamps from ikea as well as others I find it hard to figure out what lamp may be preferable for my hobby projects at home. I recall seeing a documentary where it was suggested that plants prefer red and blue light because that is the colour they themselves do not emit back. This makes me wonder why the ikea lamps don't have these colors.

I'm new at this field but I may be interested in investing in some lights for some indoor hobbying. When considering this though, what are properties of these growth lights that are important as far as plant growth goes?

In my particular situation I am not concerned with heat but more the correct type of light and the costs of electricity.

I am not a biologist, but I have read up on this a little bit. I recommend that you do a bit of research online at your library or online because it can get somewhat technical. There are several variables to consider. You are correct that the bulbs emit different colors of light. Plants species may have different needs for different colors during their growth stage & their flowering /fruiting stage. You should investigate what your plant needs. The amount of the light emitted by the bulb is measured in a unit called lumens- this is usually on the package. More lumens= brighter light. For indoor hydroponic, there are expensive lighting systems using a variety of bulbs & lamps, like fluorescent, halide & sodium, each with specific uses & (dis)advantages. One recent development are LED grow lamps. The LED's advantage is that instead of having 1 large heavy & hot light bulb like with a halide or sodium lamp, you have many little LED light that can come in different colors, allowing flexibility in different life stages. The LED lamps also consume much less electricity & don't create a lot of heat- but they are more expensive. OK, good luck with your project. Also, if you like hydroponics, learn about aquaponics, an offshoot of hydroponics that incorporates an aquarium into the system. The water flowing through the plant's roots circulates down into the aquarium and back up again, so that the fish poop helps to nourish the plants and the plants' roots act as a filter for the aquarium water, creating a type of symbiotic ecosystem between the plants & fish.


Bats observed hunting insect prey - any evidence of "handedness" (laterality) in circular flight pattern? Whilst watching a bat hunting on the wing at dusk (most likely was a species common to my urban UK location, e.g. pipistrelle) its flight pattern around the garden comprised circles, several metres in diameter, but I'm reasonably sure going in the same direction - in this case it seemed always to be turning to its left. (The circular flight pattern is something I've observed many times.) Is there any evidence in bats of a preferred direction of circular "sweep" whilst hunting? More generally, are bats known to exhibit left/right- handedness (or laterality in technical-speak) and does/could this manifest itself in flight patterns?
What I've already tried to answer my question:
Searched this site for related questions/answers + tried Internet searches with variations on circular flight for bats- results included a 2013 Nature paper, Bandyopadhyay, P., Leinhos, H. & Hellum, A. Handedness helps homing in swimming and flying animals. Sci Rep 3, 1128 (2013). https://doi.org/10.1038/srep01128 - fascinating stuff re. handedness and advantages for homing, but the brown bat featured was trained and observed under controlled lab conditions. Hoped that someone here with knowledge of the subject could provide a research paper/book ref., etc. I posted this question out of simple curiosity - I'm not a biologist and so don't have institutional access to many papers (just the Abstracts).

This article shows a lefthanded bias for climbing and eating, with one bat species:
Paolo Zucca, Alessandra Palladini, Luigi Baciadonna, Dino Scaravelli.
"Handedness in the echolocating Schreiber's Long-Fingered Bat (Miniopterus schreibersii)"
Behavioural Processes,
Volume 84, Issue 3,
2010,
Pages 693-695,
ISSN 0376-6357,
https://doi.org/10.1016/j.beproc.2010.04.006.

Paywalled - only the abstract is visible.

Found using Google Scholar with search terms: handedness, microchiroptera


Thin layers or laminae that make up a single summer band in tree ring, what are they? I took the photograph below of some tree rings. Each division on the ruler is 1 millimeter:

Each tree ring (the areas between the pizza crusts) represents one seasons worth of growth. The growing season is from about March to October. My question is about the small lamellae or dark bands that make up each ring. I have placed a green box around one set of these bands. What are they?

These small bands all seem to be the same width, so tree rings that are wider (good years) have more of them, and rings that are narrow (drought years) have fewer.

What are these bands?

Not as a confident answer but as a comment... to provide image.

The wood TS looks like ring-porous, Oak (Quercus sp.) wood (Not as identification but anatomical features are comparable).

The dark bands (radial here) seems to be xylem fibres, and bright bands (radial here), seems to be xylem parenchyma.

This is a magnified image of wood of post oak (Quercus stellata). .
Source, URL http://www.wood-database.com/wp-content/uploads/post-oak-endgrain-zoom.jpg

where it seems to me

If there is anything wrong in my knowledge, inform me and feel free to downvote this answer. If any better answer comes, I'll delete this answer.


Why do animals use glycogen for their polysaccharide storage whereas plants use starch? The polysaccharide storage form of glucose in animals is glycogen, whereas in plants it is starch. Both of these are polymers of α-glucose with α-l,4 glycosidic linkages and α-l,6 glycosidic branch points (Wikipedia article on polysaccharides). The only difference that most sources mention (e.g. Berg et al.) is that glycogen contains more branches than starch.

It is not clear to me from this information what effect the different branching would have on the structures of the polysaccharides, nor why one rather than the other would be preferred in animals and plants.

well glycogen can be broken down into sugars a lot faster, many more branches means many more ends to clip individual sugars off of, that's how you mobilize the sugar for use, it is clipped of the end of a strand. With many more branches glycogen can mobilize more sugar more quickly.  This is not important in plants but in animals that need to be able mobilize lots of energy in a hurry, glycogen works better. Additionally glycogen is a smaller molecule and easier to make, not surprising since glycogen is the ancestral condition for plants and animals.

As for why plants switched to starch, or more precisely gained it through symbiosis, starches folded crystalline structure makes it a higher density energy store but also slows its release, it is however more stable, which is important if you are going to be storing it for a long time. Animals would likely switch to starch too if they did not have to break it down to digest it, just because they take in so much of it. But since they have to break it down there is no real incentive the build it back into starch when glycogen has some advantages and quite frankly since the pathway is already there and evolution has a lot of "eh good enough".


Can a human cell live indefinetely in a controlled environment? How long can a human cell live in a controlled environment, given all necessary nutrients, temperatures, mechanisms for waste removal, and other requirements are provided for? Put differently:

Can a human cell live on indefinitely?
What's the longest known lifespan recorded for a human cell in a controlled environment?

This question is at least two questions.

Dividing cells

In terms of a dividing human cell line, every time a division occurs the telomeres capping the ends of the chromosomes get a little bit shorter. Once the telomeres get short enough they act as a signal that triggers apoptosis, destroying the cell. There is some human-to-human variation in the initial length of the telomeres, but the impression I've gotten from hanging around cell biologists is that the division limit is somewhere on the order of 10-100.

There are also cells in which the activity of a protein called telomerase is upregulated. Telomerase is a type of polymerase (an enzyme that synthesizes DNA) that acts to add extra length to telomeres. Telomerase+ cells are not affected by the division limit in the normal way. Some examples of telomerase+ cells are stem cells and many kinds of cancer cells.

Stationary cells

In a very real sense, a cell "dies" when it divides. Upon division a cell splits into two daughter cells, but it cannot be said that either daughter cell "is" the original cell. So a more satisfying way to answer to the original question would be to look at how long a single cell can be kept as-is and recognizably alive (i.e. in stationary phase).

If you cheat and freeze the cell at liquid nitrogen temperatures (78 K), then there are plenty of examples of cells surviving for decades, in the sense that a culture can be stored and then thawed, and normal life processes will resume at least some of the time.

Sadly, there may not be a proper answer out there to this version of the question. A quick lit search did not turn up much. It is thought that at least some cells (in particular neurons) last for decades in the human body without dividing, although this is unsurprisingly hard to prove.


Abnormal Prolactin Level I want to know what makes the balance of the Prolactin abnormal. Is that related to the presence of a nodule near the pituitary?

The main abnormality in prolactin levels is hyperprolactinemia, meaning blood levels of prolactin above the normal range, not during pregnancy or lactation.

The major cause of these abnormal prolactin levels are tumors consisting of pituitary lactotroph cells--called prolactinomas--which secrete prolactin. This is generally corrected with synthetic dopamine analogues, as dopamine negatively regulates secretion of prolactin in lactotroph cells.

Here is a 2010 review with further detail:
http://joe.endocrinology-journals.org/content/206/1/1.full.pdf


Is it possible to pet/groom birds? I wonder if it's possible to pet a domestic crow, or an owl. Do birds respond to grooming as cats or dogs, for example? If so, then how does one pet a bird?

Birds do groom, but not like mammals do. People tend to call their grooming behavior preening. Preening removes dirt and parasites, arranges the feathers nicely, and distributes oils over the feather (very important for waterfowl.)

To answer your question better, we need to look at the specific species. Lots of birds preen each other socially, so if you wanted to pet a bird (in a way it likes) it's good to know how the species behaves.

You mention crows and owls. Crows are social so they may preen each other; they're also sophisticated (cultural) so it's hard to generalize. A 'bird nerd' on YouTube shows convincing footage of such behavior. I think family groups of crows preen each other, but I don't have a source.

Owls tend to be solitary and would not understand preening behavior from a human. A social species of owl might preen; I don't know. Of course, if you just go ahead and pet your owl like a dog, it may appear to like it. It's hard to say if it does like it...it's easy to anthropomorphize a bird with binocular vision!


How is Pseudomonas aeruginosa diagnosed? I know that P. aeruginosa is cultured on an agar plate, but which media or assays make it distinct from other Gram-negative bacteria?

Well, the answer is actually a Wikipedia search away. But from the 7th edition of the book Microbiología Médica and Todar's Online book of Bacteriology:

Nutriotional needs. Simple. Part of why Pseudomonas spp. grows everywhere is that it can metabolize a wide array of carbon and nitrogen-containing compounds. Blood agar and McConkey are enough for its growth.
Colonies. They generally show a mucoid appearence and are flat.
Respiration. Practically an obligate aerobe. Usually oxidizes glucose, but it is capable of anaerobic respiration as well, using nitrates or arginine as electron donors. The cytochrome oxidase assay is positive, unlike Enterobacteriaceae and Stenotrophomonas.
Pigmentation. P. aeruginosa synthesizes pyoverdin (fluorescent and green) and pyocyanin (blue and water-soluble). Pyocyanin is produced when the presence of iron in the media is low, however, and not all strains synthesize it.
Temperature. Its optimal temperature is 37ºC, but its survival range is quite wide, from as low as 4ºC to as high as 42ºC.
Antibiotic resistance. And to many antibiotics. The presence of beta-lactamases makes P. aeruginosa withstand penicillin, carbapenems and cephalosporins.
Odor. Cultures emit a pleasant aroma that most associate with grapes or soap.

Wikipedia does show a nice battery of tests that identify P. aeruginosa, but if I were you I would compare them to other sources.

Positive: oxidase, citrate, motility, gelatin hydrolysis, acid production (from glucose and mannitol), nitrate reduction, lipase, pigmentation (green or blue), catalase and beta-hemolysis.
Negative: Gram staining, indole production, methyl red staining, Voges-Proskaeur (?), hydrogen sulfide production, urea hydrolysis, phenylalanine deaminase, lysine decarboxylase, acid production (from lactose, maltose and sucrose) and DNAse.


Are B Cells unique to an individual's immune system? I was wondering how the body "remembers" viruses after having once overcome them, and while reading this article on the immune system (page 14, Vaccinations), I read:

  There are many diseases that, if you catch them once, you will never catch again. Measles is a good example, as is chicken pox. What happens with these diseases is that they make it into your body and start reproducing. The immune system gears up to eliminate them. In your body you already have B cells that can recognize the virus and produce antibodies for it. However, there are only a few of these cells for each antibody. Once a particular disease is recognized by these few specific B cells, the B cells turn into plasma cells, clone themselves and start pumping out antibodies. This process takes time, but the disease runs it course and is eventually eliminated. However, while it is being eliminated, other B cells for the disease clone themselves but do not generate antibodies. This second set of B cells remains in your body for years, so if the disease reappears your body is able to eliminate it immediately before it can do anything to you.

Which made me wonder, instead of vaccinating people with weakened forms of the disease, getting their B cells to activate as described, what would be wrong with growing large colonies of B cells for a given virus and injecting them into someone who has never had the disease so that one can go straight to the last sentence of that paragraph, having many of those B cells in place before the virus is ever experienced?

Remember first that the human body nearly always, although there are exceptions, rejects any non-genetically identical graft placed into it, and therefore one cannot prepare a general colony of B-cells to confer immunity to the population at large. However, in principle, there is no impediment to removing B-cell progenitors in an individual, conditioning them to produce antibodies (which would be an artificial analogue of the natural process of 'Clonal Selection'), and re-injecting these differentiated B-cells into the patient. To my knowledge this process is currently beyond the capacity of our current cell culture techniques, as B-cell differentiation is controlled by an elaborate cell-signaling process, and even if it was feasible, it would remain impractical for several reasons. First, since the B-cell products, antibodies, can be transferred humorally, and should be tolerated by the general population, many existing treatments simply involve injecting antibodies into the patient's bloodstream. Examples of antibodies taken from volunteers' sera are the RhoGam preparations as well as IgG mixtures used to treat certain forms of immunodeficiency. There is a means of growing B-cells in culture to produce antibodies of precise specificity (i.e. monoclonal antibodies - note that clonal selection occurs in a living host for this technique, the B-cells are subsequently harvested then immortalized in culture). Adalimumab is a therapeutic monoclonal antibody.

There is however, very promising work being conducted involving T-cell vaccination, which is technically similar to what you described. The advantage in using T-cells is that these leukocytes can orchestrate an immune response, mobilizing the several, diverse elements of the immune system to respond to a specific antigen. These techniques are being principally researched as cancer treatment regimens.


Y chromosome changing sex ratios Fisher's principle explains why sex ratios in most sexually reproducing species is approximately $1:1$. However, given that in humans and many other animals, males and females differ genetically, it seems that this should cause issues for Fisher's principle.
Say that the Y-chromosome of an animal had a mutation that increased the ratios of males to females produced by the animal. At the extreme, we could imagine a mutation such that the sperm of the animal only carried Y-chromosomes. Although, by the Fisher principle, this would be bad for the overall number of offspring produces by the animal, it seems it would be good for the Y-chromosome itself, since it will now be present in all descendants of the animal (since they are all male), rather than only half the descendants. I would therefore expect that such a mutation would spread, skewing the sex ratios away from $1:1$.
Have scenarios like the one I outlined above actually occurred in species? If not, why not?

This sort of thing absolutely happens; useful search terms are "sex ratio distortion", "segregation distortion" (i.e. modifying the ratios with which different chromosomes segregate), and "meiotic drive" (a specific form of segregation distortion).
Your scenario (Y-chromosome genes forcing all offspring to be male) is much less common than the reverse (X-chromosome genes, or other genomic elements, forcing all offspring to be female), because it's easy for an all-female lineage to maintain itself by parthenogenesis. Lyttle (1991) says:

Strong Y drive is of necessity transitory, since drive
suppression must either evolve very quickly or the population will be pushed
to extinction. This may explain why few Y drive systems have been observed
in nature.

However, Lyttle goes on to describe

W-chromosome drive in butterflies (in butterflies, females are the heterogametic sex — the sex chromosomes are Z and W, ZZ individuals are male and ZW individuals are female). So this is a little bit like your Y-chromosome example, except that the populations end up all-female rather than all-male
male drive in mosquitoes

Jaenike (2001) says

Although several species exhibit Y drive, X drive is far more common.

Table 1 in that paper lists Y-drive examples in houseflies, mosquitoes, medflies, lemmings, and field mice. (I would include an image, but the table extends over 4 pages ...)

As for your final question,

I would therefore expect that such a mutation would spread, skewing the sex ratios away from 1:1 ... Have scenarios like the one I outlined above actually occurred in species? If not, why not?

I haven't dug through all the original literature that Jaenike (2001) cites, to see if there are populations in nature that are male-skewed due to selfish Y chromosomes. The point that Lyttle makes is that, even if you can find evidence of the existence of selfish Y chromosomes hiding in the population, it's very unlikely  that these will persist in natural populations for very long, because of the strong selection against them at the population level (and from the rest of the genome); either the population will go extinct, or moderators will evolve that suppress the driving effect of the Y chromosome.

Jaenike, John. “Sex Chromosome Meiotic Drive.” Annual Review of Ecology and Systematics 32, no. 1 (2001): 25–49. https://doi.org/10.1146/annurev.ecolsys.32.081501.113958.
Lyttle, Terrence W. “Segregation Distorters.” Annual Review of Genetics 25, no. 1 (1991): 511–81. https://doi.org/10.1146/annurev.ge.25.120191.002455.


How the size of ribosomes are calculated? When I was studying microbiology, something didn't make sense to me. We all know ribosomes have two subunits; the large subunit and the small subunit. Such as for eukaryotic cells, the large subunit has 60 S (svedberg) and  small subunit has 40 S. When they combine with each other they are considered as 80 S. Why it is 80 S instead 100 S?

Because Svedberg is not a measure of weight, but it is a measure of a relative sedimentation after centrifugation.
"It is defined as the ratio of a particle's sedimentation velocity to the acceleration that is applied to it (causing the sedimentation)."
The high number of S are correlated to the shape of the particles as well.

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