Have we ever observed fertile offspring with a different number of chromosomes than the parents? Chimpanzees are supposedly the closest relative of humans from a DNA perspective, they are both diploid, and they both undergo meiosis. However, chimpanzees have 24 chromosome pairs while humans have 23.

Have we ever observed a situation where the offspring of meiosis has a different number of chromosome pairs than the parents, the offspring lived, and the offspring was not sterile? How does evolution explain the shifting of chromosome pair counts?

[..] have we ever observed a situation where the offspring of meiosis has a different number of chromosome pairs than the parents, the offspring lived, and the offspring was not sterile?

Yes!

While it may seem a detail, the difficulty is to know what exactly you mean by observation. Chromosomal abnormalities, gene duplication, chromosomal duplication, robertsonian translocations, whole genome duplication are not super common but common enough to be seen repeatedly. We see them happen again and again in different lineages, we can even investigate how our environment affect such chromosomal abnormalities (Merkatz et al. 1984). So below, I am citing a few papers that I more or less randomly selected among the decently large amount of work on the subject.

Chromosomal rearrangements are sometimes involve in speciation (Rieseberg 2001).

There are many genetic disease in humans that are related to such chromosomal duplication (e.g. Down Syndrome) and de novo mutations for these mutations, while rare, are not so rare that we can witness them only on geological time scale (Veltman and Brunner, 2012)

There are soo many articles on the question that I don't really know what to cite. Of course, there are reviews that can be of interest to you (such as Zhang 2003). I tried to find a video showing a meiosis leading to chromosomal duplication but unfortunately, I have failed to find that.

The mechanisms of these mutations leading to chromosomal rearrangements are pretty well understood. You should probably start with wikipedia > gene duplication # Mechanisms of duplication for an intro.

As you talk about the difference between the number of chromosomes in chimpanzee and humans, you might want to have a look at the post Evolutionarily speaking, why do humans have 46 chromosomes where it is explains (with plenty of citations) how did the change in chromosome number occurred in our lineage.

  I have read a lot about the idea of evolution

I do not want to seem pedantic but given that the vocabulary that you are using (change in kind,  concepts of transfer errors, concept of gradual change) it really suggests that all you read comes from the creationist propaganda and not from the evolution literature. Indeed nobody use these terms in the research. Those terms are mainly used as straw man from the creationist propaganda.

There are many free intro courses to evolutionary biology. You might want to have a look at Understanding Evolution by UC Berkeley.


Other than Acetylcarnitine what other orally-bioavailable Acetyl donors exist to assist in the conversion of CoA to acetyl-CoA? I asked a question on bio stackexchange a few days from which I was hoping to be able to arrive at an answer for this question myself but I have had no such luck so now I am going to just ask outright: other than acetyl-L-carnitine are there any orally-bioavailable compounds (in particular orally-bioavailable to humans)  that exists that can serve as an acetyl group donor for CoA?

My main motivation for asking this question is that I know that acetyl-L-carnitine indirectly promotes the acetylation of histones by serving as an acetyl donor for CoA by serving as a substrate for carnitine O-acetyltransferase and then this resulting acetyl-CoA then donates an acetyl group to histones by means of the enzyme histone acetyltransferase.

This is only a guess, maybe acetic acid, ie vinegar?

Acids are effectively hydrogen salts, but the acetyl ion might be alkaline like the hydroxyl ion, making acetic acid less acidic than most? As in water, pH neutral, is a combination of hydrogen and hydroxyl, H and OH, ions?


Why do women have less synapses / neurons / brain mass than men despite having the same average IQ? I don't mean to cause offence or suggest than men and women shouldn't be of the same intelligence — that's not something I'm here to dispute. What I want to understand is how this is possible given the vastly lower average synaptic / neurone count and weight in the average female vs male brain, in terms of both the overall brain and the neocortex.
Are there some systems that the female brain employs to compensate for a lower number of neurons, and if so is it dependent to the hormone estrogen or is it something inherent to the female brain? Is it just the case that the male brain has vast redundancies, if so why does brain weight correlate with IQ if it is redundant? Or perhaps it's the discrepancies in synapse count do not extend to areas that are most closely linked with higher order thinking. This is the explanation that I am leaning to, and if someone could explain which areas these are and link to a study that shows that the male vs female average in these areas are the same, then that would be greatly appreciated (I'm not looking for areas that are the same size adjusted for total body weight, I'm looking for areas with the absolute same number of synapses/neurones).
Studies:
Female brains on average lighter than male brains: https://pubmed.ncbi.nlm.nih.gov/8072950/
Female brains on average have lower neocortical neurone count than male brains:
https://pubmed.ncbi.nlm.nih.gov/9215725/#:~:text=The%20average%20numbers%20of%20neocortical,brains%2C%20a%2016%25%20difference.&text=Sex%20and%20age%20were%20the,no%20influence%20on%20neuron%20number.
Female brains have on average a lower cortical synaptic density: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567215/
Context:
I am transgender (and taking estrogen) and have read that taking estrogen can move brain volume and weight closer to average "female proportions" to quote the study, and that this does not appear to negatively affect cognition. So, this is a question that is hugely important to me and does not come from a place of mal-intent.

In brief, so far as we can tell size matters far less than brain architecture.
Consider that humans have only about half as many cortical neurons as a number of whales, yet are clearly far more intelligent.
While we are still far from a complete understanding of the details of how intelligence actually works, neuron count is only part of the story.
For humans in particular, there is also a selection argument that would lead us to expect that relatively small differences in neuron count (e.g., between male and female average) are not particularly significant. General intelligence (not "IQ") appears to be a critical aspect of human selection, and thus under significant evolutionary pressure for both sexes. If a small adjustment in neuron count made a significant different in intelligence, cranial and cortical scale is a relatively simple morphogenetic adjustment, and we would expect both sexes to scale until they hit a more similar scaling boundary. Since that has not happened, it is reasonable to conclude that neuron count is at least not a major factor in intelligence.


Would Bubling Oxygen Through "Dead Zones" Like A Fish-Tank Make Much Difference? I am a dilettante when it comes to dead zones. I realize that they vary from fleeting algal blooms to continuous dead zones. For the continuous dead zones it would seem to me that adding a "bubbler" like for fish tanks might help restore the depleted oxygen content, which would increase microbial activity and thereby increase the quantity of nitrogen removed from the water (hopefully) before it reaches the open ocean where the fleeting algal blooms occur. Has this been investigated or could it at least be assessed from a scientific perspective?

Actually, if you could get the oxygen in there, you would probably turn the dead zone into a "feast zone," because all that algae would be food.  But I think it would be prohibitively expensive.  Fish tanks aren't deep, so it doesn't take much pressure to force air bubbles into the bottom.  And they're not large in volume, so you don't need huge amounts of air bubbling.  Oceans, or even rivers or harbors, would be another matter.
Also, some of the algal blooms are poisonous "red tides."


What is the dependent variable of a relative fluorescence graph? So it was asked what was the dependent variable of this experiment. I know that as students, we're wired to think that the y-axis is the dependent variable while the x-axis is the independent variable (probably good that way, I dunno).

However, I thought that the dependent variable in this kinetics would be time. Since this has relative fluorescence from 100 to 0, isn't the change in fluorescence for all four conditions the same, while the only affected variable being rate (which in this experiment is more dependent on change in time)?

Sorry I can't give more information about the conditions of the experiment, it's a test question that I wouldn't be allowed to post, which is why I whited-out the conditions of each line. Any help would be greatly appreciated.

When a variable is independent, it's not affected by any other variable. Relative fluorescence obviously depends on the time parameter in this case. If you stopped at 30 minutes and took readings ever 3 minutes, your data would look very different.

Without more information about the experiment, however, it's hard to tell if there are additional variables.


Survival of streptococcus after my scarlet fever I'm currently sick because of scarlet fever but I got treated with antibiotics. I know that after 1.5 day using antibiotics the streptococci I release at home are dangerous anymore. But my question is, what about the streptococci I've spread before? I've read that Streptococcus pyogenes can survive 3 days to 6.5 months outside the host, does that mean, I have to disinfect the whole house? And if so, with what should I desinfect? I worked heavily on the laptop, how do I desinfect that? Thank you.

The Streptococci are a part of the normal human flora.

  The streptococci are widely distributed in nature and frequently form part of the normal human flora (seeTable 29-1). Approximately 5-15% of humans carry S pyogenes or S agalactiae in the nasopharynx.

Please see:http://www.ncbi.nlm.nih.gov/books/NBK7611/#!po=51.4706 for more details on epidemiology of streptococci.

As 5-15% humans have it in their nasopharynx, it is not really possible to maintain streptococci free environment. It will get repopulated quickly.

Usually the reason you get infected is because of some alteration in your normal flora.

  S pneumoniae and, to a lesser extent, S pyogenes are part of the normal human nasopharyngeal flora. Their numbers are usually limited by competition from the nasopharyngeal microbial ecosystem and by nonspecific host defense mechanisms, but failure of these mechanisms can result in disease. More often disease results from the acquisition of a new strain following alteration of the normal flora. (From the same article, under pathogenesis)

So basically disinfecting wont help much as humans have the streptococci as a part of their normal flora. And it is very likely that the people you live with or come in contact with regularly have the streptococci already in their flora (either they got it from you or they originally had it themselves).


What is a DNA clamp exactly? I used to think that a DNA clamp is a protein. But today I noticed it doesn't appear in this picture. Then I went to it's Wikipedia page, where it was written:

  A DNA clamp, also known as a sliding clamp, is a protein fold that
  serves as a processivity-promoting factor in DNA replication. As a
  critical component of the DNA polymerase III holoenzyme, the clamp
  protein binds DNA polymerase and prevents this enzyme from
  dissociating from the template DNA strand. The clamp-polymerase
  protein–protein interactions are stronger and more specific than the
  direct interactions between the polymerase and the template DNA strand

Which I find a little confusing. For now it seems to me like DNA clamp is a subunit of DNA Polymerase and it doesn't have any function by itself and it is not an actual protein but it binds to Polymerase and becomes functional. Can somebody please clarify this matter to me?!

Your partly right both ways.  In a sense, the DNA clamp is a protein, in another sense, it's only part of a protein.  What it actually is is what we call a protein sub-unit, which is a protein, but which binds with other protein sub-units to form complex proteins.

In order to understand this, you have to remember what a protein is.  A protein is, in essence, a chain of amino acids.  Those can be short chains, long chains, medium chains: but they're all proteins.  Sometimes, a few short proteins (sub-units) will bind together to form one long protein (protein complex).  This is what happens in the case of a DNA clamp.

Basically, the DNA clamp is (an) independent protein unit(s) which has (have) the ability to encircle the DNA strand and travel along it.  They bind to the polymerase, which is why you don't see them on your diagram.  Their function is, very simply, to make it possible for the polymerase to stay closely attached to the DNA stand.

Sources:

DNA Repair (Amst). 2009 May 1; 8(5): 570–578


Biology experiment with algae method help I'm planning a biology experiment I need to complete. I was planning on measuring the affect of pH on algae growth. I chose chlorella to be the test algae I use (are there any algae that would be easier to test?) and I have no idea how to measure the growth. My school does not have a spectophotometer, just basic biology and chemistry stuff. Also how can I change the pH of the water for my different samples? I'm a beginner and don't really have much experience so any help is appreciated!

For growth you could measure the mass of algae before and after the experiment. If you have a centrifuge you can pellet the cells or use a filter to remove the culture medium. Alternatively, if you have access to a hemocytometer and a microscope, you could get an accurate cell count that way.

For controlling pH, you'll need a buffer in your culture medium. You should select a buffer with a pKa close to the pH you want to test and then titrate the pH of the medium with a strong acid or base (HCl or NaOH). Make sure to check the pH before and after the experiment to be sure that it didn't change due to growth of the algae.


Why do Arctic predators accumulate vitamin A? Top predators in the Arctic are known to accumulate vitamin A, often to levels that are toxic for human consumption.  A 2012 study by Senoo, Imai, et al. found that the livers of several predator species in the Arctic showed much higher levels of vitamin A than other Arctic species or closely related continental species, with no symptoms of hypervitaminosis A.

Why is it that these species accumulate vitamin A?  Does this have something to do with the food sources available in the Arctic as opposed to the mainland?  Or are there physiological reasons why Arctic predators would tend to accumulate vitamin A rather than breaking it down or otherwise eliminating it?

References:

Senoo, Haruki; Imai, Katsuyuki; Mezaki, Yoshihiro; Miura, Mitsutaka; Morii, Mayako; Fujiwara, Mutsunori; Blomhoff, Rune (2012). "Accumulation of vitamin A in the hepatic stellate cell of arctic top predators". Anatomical Record 295 (10): 1660–8. doi:10.1002/ar.22555. PMID 22907891.

The phytoplankton at the bottom of the food chain have high levels of vitamin A and precursors like beta-carotene.  At each step up the chain, vitamin A bioaccumulates.  Top predators in the Arctic deal with this by storing the vitamin A in the liver (bears, cetaceans) or blubber (pinnipeds).

This is the same mechanism that causes accumulation of pesticides like DDT in animals.  https://en.wikipedia.org/wiki/Bioaccumulation

Carotenoids are part of the photosynthetic system, and also protect the organism from sunlight.  Phytoplankton are unicellular, so each cell needs protection.  Therefore land plants contain much less carotenoids, since most of the cells are interior and protected from the sun.  For example, grains, roots, and wood have very low levels of carotenoids.

This occurs in polar regions due to up-welling nutrient-rich waters supporting high productivity.  Temperate and tropical deep ocean regions are typically deserts due to low nutrient levels, particularly iron and fixed nitrogen.


Does the deletion of Chromosome 20 cause immunity against prion disease? I was reading recently about prion disease and it caught my attention that a normal prion protein is coded n chromosome 20, therefore, in order for an infectious prion protein to attack, there must be already normal unsedimented prion proteins, does that mean the deletion of chromosome 20 in meiosis lead to immunity against prion disease, since the protein is not coded, that is if the human survives without chromosome 20

I see one report of a viable autosomal monosomy,

(https://www.nejm.org/doi/full/10.1056/NEJM196710122771502)

but in general, they are not survivable.

https://www.ncbi.nlm.nih.gov/pubmed/4086989
https://www.biology.iupui.edu/biocourses/N100/2k2humancsomaldisorders.html
https://www.ncbi.nlm.nih.gov/pubmed/29164644

A better question would be if person with a deletion or natural knockout of that gene are susceptible to that prion disease.  Those subjects likely exist in larger numbers, though it's likely that few have been exposed to any particular prion disease.


Pippin prep kits - expiration date Do you use Pippin prep? We would like to buy it, but we need more info. What is the expiration date of kits for Pippin prep? Thanks!

According to this document (page 11) the shelf life for the cassettes is 1 year. The other ingredients (running buffer, DNA size markers, loading dye) appear to be standard reagents. Of those, the DNA size marker will probably have the shortest shelf life, but it stands to reason that the reagents should have a shelf life at least as long as the cassettes, seeing as only their shelf life is mentioned. It is possible to buy reagent replacement kits.


How many gigabases of DNA are there on earth? The human genome is about 770 MB, the C. elegans genome is about 100 MB, the yeast S. cerevisiae is about 12 MB. Different other genomes have been sequenced: how many GB of genomic DNA we have now?

Let say we would like to make a Noah hard-disk ark: how much space would it take to represent the genomes of all known species on earth? There is a way to provide an estimate?

I'm also interested in the total biodiversity: for instance, if two species each have 1 GB genomes and have half of their DNA in common this would count as 1.5 GB.

If you simply take one order of insects, Coleoptera, there are just under 400,000 described species with estimates from 850,000 to 4,000,000 species total in just this order.  The number of primates is under 1,000.  If your assumption of say 10MB for all other primates would be accurate, just adding in the low end estimate of 850,000 at 10MB per 1000 we are quickly at 8,500GB which seems to be a factorial out of the GB range.

So, we have a broad estimate of non-bacterial of plants, animals etc. at say 8,700,000.

Jason Gans found in a 1 gram of soil survey approximatly 1,000,000 bacterial species.

SO the total accounting for species number is totally impossible to estimate for anything at this time, let alone the genome.

Even for something as "common" as a giraffe, there are up to 9 sub-species with genome differences within each subspecies.

So, once we get them all decribed, we can then work on the genome sequence for each and get you some answers!


Can genes that activate transcription factors also called be called transcription factors? If the sole known function of a gene is to activate a transcription factor, would that gene also be considered a transcription factor, or is there a word for such genes that are further upstream on the transcription activation cascade?

Yes.  For an example, see this list of targets of NF-kB (a transcription factor).  Many other transcription factors are included there.  As for a TF that does nothing except activate another, single TF?  I don't know that those exist - TFs tend to modulate multiple genes.


Recommendation for a molecular biology book that explains how we know what we know My background is in math and I know very little about biology.  The few biology books that I've looked at seem to explain what is known (or what is believed), but don't really explain how we know what is known.  For a specific example, when I hear that "DNA makes RNA and RNA makes protein", I would like to know things like:

How do we know that DNA makes RNA?
How do we know that RNA makes protein?
How do we know that there is such a thing as "protein" in the first place and how do we know what it is?
How do we know that there is such a thing as RNA and how do we know what RNA is?

Can you recommend any books that do a good job of explaining how we know what we know in molecular biology and genetics?

This is not my favourite book on molecular biology (Alberts is my favourite, and Lodish is the runner up), but I'd recommend The Cell, A Molecular Approach, by Geoffrey Cooper

This book has, for every chapter, one or more boxes called "Key Experiments", in which the author describes famous experiments that allowed us to know what we know now about that subject.

For instance, at chapter 10, titled "Protein Sorting and Transport", the Key Experiment box shows the discovery of the peptide signal by Gunter Blobel:

And the best news, the book is completely free at NCBI bookshelf:

https://www.ncbi.nlm.nih.gov/books/NBK9839/

It's searchable, but unfortunately not browsable. However, the workaround is very simple: just type the chapter title in the search box!

Of course, some concepts are so old (for instance, you asked "how do we know that there is such a thing as "protein" in the first place") that you probably are not going to find them in molecular biology textbooks, but on a book about history of science instead.

PS: By the way, both Alberts and Lodish are also free to read (and browsable) at NCBI bookshelf!


What is the term for awareness of or inclusion of real sounds within a dream? I fell asleep while listening to a podcast, and I am sure I was dreaming but I could also still hear the podcast.

The podcast played an important role in the dream, I was searching for the source of the voice, wondering if others in the dream could hear the same voice. I started to feel a bit panicky and woke up as the podcast also happened to end. I rewound the show and confirmed that it was all there, exactly as I had heard in my dream!

I would like to read more about this type of experience, but I am having trouble finding the right words to search. Is there a name for this phenomenon? Is there anything that contributes to experiences like these? I know it wasn't lucid dreaming, because I wasn't aware of being asleep.

I think I found a good expression : "sensory incorporation in dreams"

https://www.psychologytoday.com/blog/dream-factory/201409/sensory-incorporation-in-dreams

It doesn't seem reflected in a Google Scholar search however, and I don't find a consistent terminology in the papers that do seem to be about the subject. That article can be a good starting point though.

EDIT: other good one: "influence of external stimuli on dreams".

https://journals.ub.uni-heidelberg.de/index.php/IJoDR/article/view/15754


Pasteurization and Bioavailability of Antioxidants in Beet Juice What are the effects of pasteurization on the antioxidants found in beet juice ? Does the process render most of the beneficial nutrients (betaine) useless and make them unable for the body to process as efficiently as it would with raw beet juice? Also, does the pasteurization process do this to most fruit and vegetable juices ? I appreciate any insight, I've seen a lot of conflicting reports and am curious of anyones thoughts. Thank you

So, when they subjected "ready to drink" beetroot juice to thermal pasteurization, they found the betacyanin and betaxanthin (our major antioxidants, and pigment molecules) content to be 39.9 and 42.28% degraded, respectively (1). Their conclusion was as follows:

  Standardization of process condition and
  quality degradation of beetroot juice due to thermal
  pasteurization was studied. The standardized T2
   batch
  with total heating time (fh) of 720 s thermal in-pack
  pasteurization leads to the minimal degradation of
  color, betalain content (Betacyanin and Betaxanthin),
  antioxidant activity and complete inactivation of
  micro flora of beetroot juice. The color, betalain
  content (Betacyanin and Betaxanthin) antioxidant
  activity and sensory of the beetroot juice was
  significantly (p < 0.05) reduced during 180 days
  ambient (27-30°C) storage, but still the quality of the
  juice was adequate upto 180 days. We concluded that
  thermal pasteurization of 96 °C for a total heating time
  (fh) of 720 seconds with P-values of 11.16 would be
  a good method to produce microbiologically stable
  beetroot juice with the retention of quality attributes.

So our goal is to get a juice that retains as many "good" attributes as possible, while producing a product that isn't going to get anyone a foodborne illness. As for the net effect of pasteurization on fruit juice in general, im still coming to a conclusion there. The process shouldn't render too much of the fruit/vegetable ineffective, though I'd still expect some degradation either in storage or processing.


Evolution of dinosaurs What did dinosaurs evolve from? Was it the reptiles that evolved from amphibians? I have been researching this but am very confused with who their direct predecessor was. Amphibians evolved from fish...reptiles from  amphibians...dinosaurs from reptiles (?)...and birds from dinosaurs. That is my understanding, but it could be wrong. How are dinosaurs related to reptiles? And if they did evolve from reptiles, which kind of reptiles (such as lizards, crocodiles, or turtles for example)?

Source of information

See the post The best free and most up to date phylogenetic tree on the internet? for info about how to find such information.

Generally speaking, you might be interested in an intro to phylogenetics such as the one provided in this answer for example.

Where are dinosaurs in the tree of life?

Dinosaurs fall within the Reptiliomorpha clade. Please note that Reptiliomorpha does not quite correspond to what we today call reptiles. Please see the post If dinosaurs could have feathers, would they still be reptiles?

Reptiliomorpha is the sister clade to Amphibia (from here) which contain all living amphibians.

If you look within the Amniota, you will find all of the following

Here, you see that turtles and mammals are an off-shoot of Diapsida. So dinosaurs are not mammals and there are not closely related to turtles. Now if you click on Diapsida you will find ...

the Archosauromorpha which contains all crocodiles, birds and dinosaurs. You can keep going to find Therapoda which contains many dinosaurs and birds. You can keep going like this for yourself and discover the entire tree of life!

Reacting to your sentences

  What did dinosaurs evolve from?

When asking this question, please do not forget that no species evolved from an extant species. If this is unclear to you, you should have a look at this post.

  Was it the reptiles that evolved from amphibians?

Well... the term reptile is a mess because it does not represent a monophyletic group (see this post). If you do not understand the term monophyletic, then you should have a look at this answer.

  Amphibians evolved from fish...

Well... sure. However, fish is also not monophyletic so it is misleading. Also, I am afraid when you say "Amphibians evolved from fish" that you are thinking of modern extant fish which would be wrong.

  reptiles from amphibians...

Nope, this is wrong. Reptiles and amphibians are sister(-ish) clades.

  dinosaurs from reptiles (?)...

This is more or less true although again, do not think of modern reptiles and also, reptiles is a mess because it is not a monophyletic group. But Dinosaurs are Reptilia

  and birds from dinosaurs.

Yes, this is pretty much true.

Note generally though that it is misleading to say "birds evolved from dinosaurs", "humans evolved from apes" and "mammals evolved from vertebrates". It is more correct to say "birds are dinosaurs", "humans are apes" and "mammals are vertebrates". I would be even better to use the latin names to avoid confusion with misuse of these words in the popular culture.


What Proteins Are Universal To All Life Forms? According to National Geographic, there are 23 proteins that are common to all life forms:

  All species in all three domains share 23 universal proteins, though the proteins' DNA sequences—instructions written in the As, Cs, Gs, and Ts of DNA bases—differ slightly among the three domains

According to NCBI there are 324 proteins common to all life forms.

How many proteins are common to all life forms, and what are their names?

This question is based upon a wrong inference about the work that forms the basis of the National Geographic article, which includes this statement:

  All species in all three domains share 23 universal proteins, though the proteins' DNA sequences—instructions written in the As, Cs, Gs, and Ts of DNA bases—differ slightly among the three domains (quick genetics overview).
  The 23 universal proteins perform fundamental cellular activities, such as DNA replication and the translation of DNA into proteins, and are crucial to the survival of all known life-forms—from the smallest microbes to blue whales.

The article is referring to a paper published in Nature in 2010.

http://www.ncbi.nlm.nih.gov/pubmed/20463738

This paper uses a set of 23 proteins to test the idea that certain genes arose only once.

  The data set consists of a subset of the protein alignment data from ref. 27, containing 23 universally conserved proteins for 12 taxa from all three domains of life, including nine proteins thought to have been horizontally transferred early in evolution27. The conserved proteins in this data set were identified based on significant sequence similarity using BLAST searches, and they have consequently been postulated to be orthologues.

There is no suggestion that there are only 23 such proteins, it's just that the author chose this subset to test his ideas.

And here they are:

  alanyl-tRNA synthetase, aspartyl-tRNA synthetase, glutamyl-tRNA synthetase, histidyl-tRNA synthetase, isoleucyl-tRNA synthetase, leucyl-tRNA synthetase, methionyl-tRNA synthetase, phenylalanyl-tRNA synthetase β subunit, threonyl-tRNA synthetase, valyl-tRNA synthetase, initiation factor 2, elongation factor G, elongation factor Tu, ribosomal protein L2, ribosomal protein S5, ribosomal protein S8, ribosomal protein S11, aminopeptidase P, DNA-directed RNA polymerase β chain, DNA topoisomerase I, DNA polymerase III γ subunit, signal recognition particle protein and rRNA dimethylase


What unicellular eukaryotes reproduce sexually? By sexual reproduction I am referring to, at least, gametogenesis or mating bridges. I was previously under the impression that unicellular organisms did not reproduce sexually at all.

So far the sexually reproducing unicellular eukaryotes I am aware of are yeast, diatoms, malaria-causing Plasmodium and some diplomonads.

This addresses your original question of "simplest" versus smallest. I'm not sure of sizes.

Investigate diplomonads: https://en.wikipedia.org/wiki/Diplomonad Most notable among them is Giardia: https://en.wikipedia.org/wiki/Giardia

These critters are primitive enough to lack Golgi and their version of "mitochondria" are substantially different enough (not synthesizing ATP) to be called by another name, mitosomes. Most have two nucleii and were not even thought to reproduce sexually  until relatively recently


From what stage can you speak of an inflammation? Imagine you hit your foot at a table leg and it hurts a while or you got a tiny graze. Those injuries aren't an infection but could these things still be called an inflammation?

Is it necessary that in both cases cells are damaged to induce a cascade of hormones? Or with other words, is there always an inflammation when cells are damaged or is needed more?

From PubMed Health:

  When a wound swells up, turns red and hurts, it may be a sign of inflammation. Inflammation is – very generally speaking – the body’s immune system’s response to stimulus. This can be bacteria colonizing a wound or a splinter piercing your finger, for example. Inflammation happens when the immune system fights against something that may turn out to be harmful.

So when inflammation occurs, chemicals from the body's white blood cells are released into the blood or affected tissues to protect your body from foreign substances. This release of chemicals increases the blood flow to the area of injury or infection, and may result in redness and warmth. Some of the chemicals cause a leak of fluid into the tissues, resulting in swelling.

Signs of an inflammation :

There are five signs that may indicate an acute inflammation:

Redness
Heat
Swelling
Pain
Loss of function

There is a loss of function, for example, when the inflamed limb can no longer be moved properly or when the sense of smell is worse during a cold.

This means that an inflammation does not start when a wound has been infected by bacteria, festers, or heals poorly, but already as the body is trying to fight against the harmful stimulus or a viral infection.

Not all five signs occur in every inflammation. Some inflammations occur silently and do not cause any symptoms.

So depending on the symptoms we can decide if there is an inflammation or no.


How does plant grafting work? Plant grafting is a process whereby a piece of one plant is inserted into another and results in a change of the original plant. For example, grafting a piece of a lemon tree into a bitter orange tree will cause that tree to produce lemons instead of oranges for the rest of its life.

How does this work? I mean, at the genetic level. I guess the grafted plant is now a chimera of some sort but if so

How does the grafted DNA affect the host cells?
Are all of the host's cells affected?
If we were to sequence the grafted tree which genome would we find?
Is it perhaps that the host DNA is not affected at all and the effects come via a change in expression levels? If that is the case I would assume grafting will only work between very closely related species. Is that so?

Basically I know very little about plant genetics and physiology. I remember from my undergraduate days that plant genetics are just plain weird. Most, if not all, have various levels of polyploidy. Is that relevant?

This article analyses the exchange of DNA during the process of grafting

Exchange of Genetic Material Between Cells in Plant Tissue Grafts - Stegemann and Bock, Science 2009

Quoting from the article:

  Although the grafted tissues fuse and establish vascular connections,
  the stock (the lower part of the graft) and scion (the upper part,
  usually supplying solely aerial parts to the graft) are thought not to
  exchange their genetic materials. But grafting (whether natural or
  assisted) provides a path for horizontal gene transfer. Gene transfer
  is confined to the graft site and no long-distance transfer may occur.
  Analyzes indicating that large DNA pieces or even entire plastid
  genomes are transferred. Only plastid genes may be transferred, no
  transfer of nuclear genes occur. Plant cells are connected via
  plasmatic bridges called plasmodesmata, but the passage of large
  macromolecules requires the action of specific plasmodesmata-widening
  proteins. Whether large DNA pieces or even entire organelles can
  travel through plasmodesmata requires further investigation.

  Finally, although our data demonstrate the exchange of genetic
  material between grafted plants, they do not lend support to the tenet
  of Lysenkoism that “graft hybridization” would be analogous to sexual
  hybridization. Instead, our finding that gene transfer is restricted
  to the contact zone between scion and stock indicates that the changes
  can become heritable only via lateral shoot formation from the graft
  site. However, there is some reported evidence for heritable
  alterations induced by grafting and, in light of our findings,
  these cases certainly warrant detailed molecular investigation.


Is each blade of grass an individual plant or not? Sometimes when I do gardening, I notice multiple blades of grass appear fused together at the root, yet still appear to be segmented. When I look at images, I get some that suggest each blade is an individual plant like this one, and I find ones that suggest they're fused together like this other one, and I wouldn't know if they're actually fused or if they just have a tendency to have seeds or roots distributed in a clumped manner as some survival strategy.

Should it be assumed that each individual blade of grass is a separate plant, or otherwise how many blades are part of the same plant?

Each blade of grass is part of the grass plant and may have multiple blades.  Clumping grasses, when mature, can spread producing multiple shoots with additional blades.  The number of blades would depend on the type of grass and individual seed, but the clumping grasses tend to produce 10-16 leaves/blades.

Source: Poaceae - Wikepedia


Is there a reference for the composition of viral genomes? First of all forgive me for the bad written question.

I'm not a biologist. I'm neither a doctor nor a virologist. I am a physicist actually, and I have this question in mind since a long while.

What I'm trying to ask is if there is a sort of text file or a website (or a book) where I may read about viruses "composition".

"Composition" means something like

"This is the rhinovirus, and it's genetic "composition" is ACTGCT" (of course I just invented...).

I don't know how to express myself with good terms because I am not familiar with this field, so please feel free to edit the question if it may appear unclear.

Again, what I'm asking is for a sort of database of genetic sequences about viruses and so on.

Thanks in advance!

NCBI houses a collection of viral genomes at the aptly named Viral Genomes portal. They currently have 5921 viral genomes and by going to the previous link you can browse sequences from the major viral families.
If you have a nucleic acid or amino acid sequence it can be searched against NCBI's sequences here.
Uniprot also have a viral protein sequence annotation project which they describe as such;

The concept of this website is to associate specific knowledge for each virus family with viral protein and genomic sequences. All the available information is presented in a concise and accessible virus fact sheet, associated with the ordered list of reviewed entries. The site covers the whole known virosphere. The database section allows access to UniProtKB protein entries, as well as to specific virology databases.
Our efforts are currently directed towards viral ontology and reference strain annotation. A robust ontology will allow a more precise definition of the involvement of each protein in viral replication steps. The reference strain annotation will become the benchmark for each of the 334 genera.

Their work can be accessed through uniprot.org or through the project portal at; http://viralzone.expasy.org/


What, if any, diseases do larder beetles carry? I found one of these beetles on my bed as I was attempting to get in. I'm 80% sure my cat carried it in (I found it in the exact same space he had been sitting ten minutes previously).

My question is what, if any, diseases do these bugs carry? It did not bite me, though it may have bitten my cat. I'm more worried about bacteria etc that it may have carried around my bed/room. Can they transmit salmonella? Should I break out the disinfectant, or is it no big deal?

I have researched them as best I can, and I found someone noting that they can spread bacteria, but found nothing on how severe it is. For example, my cat obviously spreads bacteria, but I let him on my bed without worry. I have never see one of these beetles before.

I have a secondary question, if that's allowed - what are the chances it laid eggs on my bed? It was there for possibly 4-5 hours if my cat indeed carried it in. I have rodents (pets) in my room and am peripherally worried about an infestation happening.

For context, I live in the center of the UK.

I have never heard of larder beetles carrying any serious diseases and chances are slim that it could have laid any eggs, so you probably have nothing to worry about. If you want you can spray the area down with a cleaner, but as I said earlier, it's probably fine.


is there a way to do batch download for all gene pathways? I would like to download all the gene pathways and genes of each pathway. Preferably, gene length of each gene as well. It would be a lot more convenient if there is an R package.

Try using KEGG REST.

http://rest.kegg.jp/link/pathway/hsa ## list of all genes and pathways in Humans


Dragonish caterpillar from North Vietnam I encountered this caterpillar in North Vietnam (Hanoi) and could not find any reliable web site for this kind of search. I am not an entomologist, so I don't even know how to describe it, except that it has hairy head stalks. I hope my pictures will help.
Thanks to anyone who can help me here.

My comment above is actually likely wrong.

Instead, I think this is possibly the larva of the rose-myrtle lappet moth (Trabala vishnou) in the Lasiocampidae. (It may also be the larva of the closely-related roseapple caterpillar, Trabala pallida -- see here and here).

I don't know this group of moths at all, but a series of failed "Lymantriinae" searches and otherwise successful image searches led me to this genus and these species. Lack of reputable resources available in English online make differentiation between species in this genus very difficult for me. Below are some images of Trabala caterpillars:

 Images Source: Koh Chang Nature

You can see a very smilar image to the ones above on flickr.


Comparing gene expression levels between control and disease at different time points I have a data set with expression levels of a list of genes, measured in replicate at two different time points between two groups; a control group and a disease group.

I want to identify the changes in expression between the two groups, however I'm having some trouble on formulating how best to do this. For example, if I have $[C_0]$ and $[C_1]$ as the control group measured at $t=0$ and $t=1$ respectively, and $[D_0]$ and $[D_1]$ as the disease group, I had tried to do:

$$\frac{([D_1] - [D_0]) - ([C_1] - [C_0])}{[C_1] - [C_0]}$$

I feel like a fold change would be appropriate, however it doesn't seem to make any sense logically for the genes where $[C_0] = [C_1]$ or $[D_0] = [D_1]$.

Could anyone suggest an appropriate ratio or measurement? This is straightforward enough when it's simply comparing between C and D, (e.g. you just find $\frac{D}{C}$), however I'm not sure how to treat the different time points.

The gene expression profile may change at different time points between the two groups; you should decide what you actually want to measure. If you want to see if the diseased group is different from the control then you should compare them at every time point. For most situations you would need to compare just their steady state behaviour.

Imagine a diseased individual who shows some physiological differences at certain developmental stages compared to the control but in the end turns out to be perfectly normal. So what matters in most cases is the steady state and not the transients.

However if you are interested in the change in expression then you should compare ([D1] - [D0]) with ([C1] - [C0]). This will tell you if the dynamics of the diseased and the control samples are similar or not.

There are issues with fold changes. Though they are decent measures, you cannot really apply a t-test with fold changes (normalizing to 1 is a different thing).

You can do another t-test between [C1] and [C0] (similarly for D). This would tell you if the diseased or control population changes its expression at time t=1 or not.

AFAIK you cannot compare the dynamics and the values simulatenously. What you should test depends on what you are interested in.


Are there genes in sex chromosomes that determine facial features? My friends and I were bored enough to try out this activity.

Picture a teenage boy in your mind.
From this picture, remove any accessories (glasses, piercings, etc.), moustache or beard, then replace the hairstyle with that of a stereotypical teenage girl.
Are you possibly convinced if someone tells you that, this picture was originally of a teenage girl?

I tried it by picturing a few boys who are my friends, but still, I was never convinced because I feel that there's something inherent about the facial features of these boys that made them appear boyish rather than girlish.
If this is not some psychological effect caused by my acquaintance with the boys I pictured (as I know them well so I cannot accept the mapping of their faces to the opposite gender), then are there really biological factors, genes in sex chromosomes in particular, that result in differences in the development of facial features between males and females?
Apparently, "facial hair" isn't an acceptable answer...

Yes, having a Y chromosome does cause specific alterations to facial structure.

The Y chromosome doesn't contain much actual genetic information. Most of the information needed to activate the male developmental program (the female one is the default) is in just one gene 'SRT', the other genes on the Y chromosome aren't super important, such that you can get a normal looking (but infertile) man if this gene is transferred onto an X chromosome.

This SRT acts as a switch causing various changes, but one of the most important ones is the higher production of testosterone. Testosterone (and some other hormones called  'androgens' cause changes to a lot of things, and one of them is facial morphology. In fact weirdly, the bones in the face retain the capacity to grow in adults, so you can give someone hormone treatment and their facial structure will change (google this and you'll clearly see the difference in people's facial shape after hormone therapy for sex change procedures - especially around the jaw). There is also some correlation, in both sexes, between the amount of testosterone in someones blood and the 'manliness' of their face.

Your teenage friends are currently undergoing a natural process similar to artificial hormone treatment, and their faces will get more and more male looking as puberty goes on.


Why does my gel have such poor resolution? Brand new user to bio stack exchange here. I ran this gel (0.9% agarose, run starting at 60V then to 105V over ~30-45 min) with DNA samples containing 20uL of DNA and 1X tracking dye in each of the wells. I do not know why the resolution of this gel is so poor. I'm assuming it's from DNAse activity, as this is what my lab tech said it probably was. I'm pretty sure I did everything right regarding the procedure. I'm not sure what other info I could provide, other than the samples were prepared and stored at -20C a week prior to the gel being run. Here's a picture of the gel below.

Although your tech is referring to your DNA samples, your ladder also indicates there is some room for improvement of your running technique. -20C for a week should not have impacted the quality of the DNA assuming that it was good quality going into the freezer. You can mitigate DNAase activity by adding EDTA to your storage buffer, which will pull metal ions out of solution. Just make sure to take that into account if you're doing a reaction later that requires metal ions (like PCR).

DNA

Focusing first on the DNA samples. There are a few things to check.

How much did you load? I see you stated 20uL, but what was the concentration? It it more important to know the amount of ng being used as the sample. Various stains have different concentrations they can detect (EtBr, SYBR, etc.) I would check the specifics of the stain you're using to make sure you're loading an appropriate amount of DNA.

Are these PCR products? If so, how many cycles was your PCR run? I have seen similar results from PCR if the samples are run for too many cycles. Non-specific products begin to be produced in later cycles, and will cause degradation of your specific products. I would also re-check your primers, the extension time, and the polymerase you're using. It is more difficult to do extensions of the 5.8kb and 6.8kb sizes you mentioned, but not impossible.

Are these restriction digests? Do you have a control well showing the undigested plasmid, or other source? Your source should have a clean band first to expect a clean band in the results. If your source is clean and bright, and the digest looks like the samples above, check your digest buffer and enzymes.

Electrophoresis

There are several things which can improve the quality of an agarose gel. Thermofisher provides a guide for their tips and tricks. Below are things that I have found useful in my own experience.

The time between casting the gel and running it. A common practice is to make gels and store them in TBE/TAE buffer until they're ready to be used. In my experience, the quality of the gel will degrade over time, yielding diffuse bands. The best results are achieved with a freshly poured and cast gel.
Loading technique. Carefully loading the samples into the wells so that they settle as closely to the bottom without mixing with the surrounding buffer is key. The best results are achieved by having your pipet tip touching the bottom of the well, and slowly pulling it out as you release your sample so the sample does not have to settle down into the well on its own.
Run immediately after loading, and image immediately after running. Diffusion will cause nice tight bands to become poor the longer the samples sit in the well.
Voltage, timing, and agarose concentration. Getting these right takes practice. You'll want to try to run your gel as quickly as possible. The more time it sits in the gel, the more diffusion will occur. However, have the voltage too high, and you risk melting your gel. Vary the concentration of agarose to target the size of DNA you're after. I have previously used anywhere between 0.5% and 1.5%.
Prestaining the gel or poststaining? I prefer prestaining for the stains that work well, as it reduces the time the samples will sit in the gel allowing diffusion to occur.
I am looking at your ladder, and the link to the provided standard, and it is difficult to tell which bands are which. The 3.0kb fragment should stand out as the brightest, however the bottom band in your gel is the brightest. Is this the 3.0kb band? Maybe. It's difficult to count the number of bands above it to confirm. If it's not, which might be indicated by the fact that none of your samples seem to have run to the end of the gel, then this would be the 0.5kb band. If it is the 0.5kb band, the ladder intensity doesn't match up with your expected intensity. Double check your ladder so you can know what sizes you're looking at.


Small vs Large neurons What is the criteria for classifying neurons as small and large?
Is this classification based on gross size or the length of axon?
Do they have any physiological difference?

For instance it is said that Substantia gelatinosa of Rolando contains small neurons .

What is so special about calling those neurons as such?
Aren't they doing the same function of conduction of impulses?

I have googled it but couldn't find any explanation for such naming.

Depending on the neuron, small/large could mean one of two things:

1: Axon diameter, larger axons have lower resistance, so transmit action potentials faster see tables here. Important for neurons that cover long distances to convey information quickly.

2: What I think you mean though is the size of the cell body, where some neurons, e.g. Purkinje cells are much larger than nearby golgi cells. In which case the size is related to the function, large cells tend to have large dendritic fields and integrate many inputs into a single output, often relayed to a different area of the brain. Small cells are typically interneurons that only have an effect over a very small area.


Hamming distance between two DNA strings By definition from Wikipedia, the Hamming distance between two strings of equal length is the number of positions at which the corresponding symbols are different. In other words, it is the number of substitutions required to transform one string into another. Given two strings of equal length, compute the Hamming distance.

So to find the how many differences there are between two strings, say we have two DNA strings A and B:

A = TGACCCGTTATGCTCGAGTTCGGTCAGAGCGTCATTGCGAGTAGTCGTTTGCTTTCTCAAACTCC
B = GAGCGATTAAGCGTGACAGCCCCAGGGAACCCACAAAACGTGATCGCAGTCCATCCGATCATACA

Throw them to two arrays A and B. Therefore, If

(= count 0)
(cond
   [(symbol=? A[1] B[1]) /do nothing just move on to the next pair of string]
   [else (add1 count)] ;; counter:= counter + 1;

output would be the counter.

Is this the right logic flow to go with this problem? Any suggestion to write this on python or Scheme?

Your logic on the problem seems correct. The wikipedia article about the Hamming distance describes both a python and a C implementations. The python version assumes two strings of equal length:

def hamming_distance(s1, s2):
    #Return the Hamming distance between equal-length sequences
    if len(s1) != len(s2):
        raise ValueError("Undefined for sequences of unequal length")
    return sum(ch1 != ch2 for ch1, ch2 in zip(s1, s2))


Telomeres and daughter strands How is the primer present in the daughter, leading strand replaced? I've circled the primer in question.

I don't see how this primer can be replaced by DNA polymerase; there is no free 3' end for DNA pol to act on.

My book, however, says there is no telomere problem with the leading strand.

Other sources say there is a telomere problem.

So what is it?

Replication doesn't start at the very end of a chromosome, so there is no problem with leading strand synthesis. It's probably easiest to see if the other half of the image was there:

Forgive the lion; plain white paper seems to be in short supply. Also my writing. Too much tea this morning. Hopefully you can see that leading strand synthesis can continue right to of the end of the chromosome as the fork progresses. The leading primers at the replication origin can be replaced once the first Okazaki fragment from the other replication fork is synthesized.

There is, however, a problem, aptly termed the end replication problem, with lagging stand synthesis:

The dots just mean the chromosome continues in that direction. Important to notice is the lagging strand RNA primer at the end of the chromosome. When this is removed, there is apparently no way to synthesize DNA there. Repeated replication cycles progressively shorten the chromosome and cause the Hayflick limit to cell division (the number of times a cell can divide before dying). To solve this problem, some cell types express an enzyme called telomerase. This is an RNA directed DNA polymerase that adds deoxyribonucleotide repeats to the 3' end of a DNA strand, using its own internal RNA template, to prevent information loss.


Flicker fusion threshold for insect eyes I searched on bio-numbers for flicker-fusion threshold of insect eyes in general and for flies in particular. Ruck, 1961 gives values for some flies. Is there any database maintained for these values? Is there any comparative study done for many flies/insects?

"The flicker fusion frequencies of six laboratory insects, and the response of the compound eye to mains fluorescent ‘ripple’" (Miall, 1978) touches on flicker fusion thresholds for six different insect species commonly used in laboratory settings:

  Locusta migratoria, Periplaneta americana, Saturnia pavonia, Antheraea pernyi, Glossina morsitans and Drosophila hydei.

I also found this paper: Potential Biological and Ecological Effects of Flickering Artificial Light (Boyles, 2014) that includes an exhaustive literature search of flicker-fusion thresholds and other related data for many species (including insects). If you're looking for an authoritative source, I'd say that this is it (as there doesn't seem to be a database with this information).


293T safety, transfections with plasmid DNA I am a little concerned with 293T cell lines, I have been working with this cell line for a few years with less frequency. However there were times that i extracted the proteins from these cell lines outside the hood. I never work with virus, i have only transfected plasmid DNA. can someone help me if there are any chance o exposure, if yes, how dangerous is it.

293T cells do incorporate partial virus genomes, consisting of about 4000 bases (about 11%, if I remember right) of the adenovirus type 5 genome (Cloning and Sequencing of the Cellular–Viral Junctions from the Human Adenovirus Type 5 Transformed 293 Cell Line).

This amount of DNA is not enough to make a viable virus; it lacks all the structural components of the capsid, for example.

293T cells also include the SV40 Large T antigen, another viral gene. Again, this is not enough to make a replicating virus.

Therefore these cells don't pose any human health hazard aside from the normal almost entirely theoretical risk associated with any transformed human cell line (actually considerably less, since these were never tumor cells but were transformed in the lab, so they have no intrinsic adaptations to replication in humans, unlike say HeLa cells -- which are also demonstrably safe).

293 cells have been continuously cultured in thousands or tens of thousands of labs for over 40 years, and I'm not aware of any safety incidents associated with them.  Of course, you should always handle cultured cells with appropriate precautions and protective wear, but these are not a specific concern.


What does "developmentally programmed" mean? What does the term "developmentally programmed" mean? I can't seem to find a definition anywhere.

What would the alternative (i.e. not developmentally programmed) imply?

The term could mean two things depending on the emphasis:

"developmentally programmed" would seem to emphasise the "programmed" nature of the development of something, implying that it is under specific regulation and the result of targeted energy expenditure ("Here, we describe widespread developmentally programmed nuclear destruction (PND) events that occur during yeast gametogenesis").
"developmentally programmed" would be intending to distinguish from other means of being programmed, i.e. this would go in the direction of a nature vs. nurture statement ("Hair colour is developmentally programmed and does not depend on external influences after fertilisation").

The first of the two appears to be the more common use of this phrasing if one wants to trust Google to be representative. Something along these lines might be intended in your example, though I don't see why this statement is necessary as it seems quite obvious that any organ that develops during embryogenesis is "developmentally programmed"...

I suppose the alternative ("not developmentally programmed") would imply that the development of secondary lymphoid organs is an accident which is not driven by specific mechanisms that exist for the particular purpose of developing them.

In any case, there is no magical scientific meaning to either of these two words, to me your example seems to be rather a mishap of phrasing.


Hodgin-Huxley model for a single neuron - continuation As  continuation to This question I have posted. Another set of questions is given for the same model :

This time it is also given that for $t<0$ the membrane potential is $u_0$, and at $t=0$ it is instantaneusly jumps to $u'$, and that $u_0,u',u_2,u_{ion}$ are maintained for $t \geq 0$.
So, with this additional data I could actually compute $r(t)$ and $s(t)$ for $t \geq 0$ in the following way:

For $t \geq 0$, $u(t)=u'$
so $r_0(0)=r_0(u') \approx 1$ and $s_0(0)=s_0(u') \approx 0$.
Also, $\tau_r(0)=\tau_r(u') = 1$ and $\tau_s(0)=\tau_2(u') = 15$.

So, we get:
$r' = -\frac{r-1}{1}$ and $s'=-\frac{s-0}{15}$ $\Rightarrow$
$r' + r = 1$ and $s' + \frac{s}{15} = 0$.

These are a first order linear diff. equation of the form:

  $y'(x)+p(x)y=q(x)$

So their solution is of the form:

  $e^{-\int{p(x)dx}}(\int{q(x)^{\int{p(x)d(x)}}}+C)$ ($C$ is a constant)

So I get:
$r(t)=C_1e^{-t}+1$ and $s(t)=C_2e^{-t/15}$.

I think that we have no way of knowing our initial conditions $r(t=0)$ and $s(t=0)$ (am I right?)
So for simplisity let's assume that $C_1=C_2=1$ and we get:

  $r(t)=e^{-t}+1$ and $s(t)=e^{-t/15}$.

So for example: $r(t=100) = e^{-100}+1 \approx 1$ and $s(t=100) = e^{-100/15} = 0.0013$ and $r(t=3) = e^{-3}+1 = 1.0498$ and $s(t=3) = e^{-3/15} = 0.8187$

So my question is:
How come answers 4 and 7 below denoted as true?

Actually there is a way to determine the initial conditions for this problem.

We assume that the gating variables $r$ and $s$ are at a steady state before the membrane potential jump from$u_0$ to $u'$.

If we look at the first graph(the steady state relation versus membrane potential) we can see that at the membrane potential $u_0$ that $r(t=0)\approx 0$ and $s(t=0)\approx 1$.

Then we make our jump in voltage from$u_0$ to $u'$ and now our $r(t)$ and $s(t)$ will change towards their new steady values $r'=1$ $s'=0$ with time constants given by the second graph.

Your equations $r(t) =C_1 e^{-t}+1$ and $s(t)=0+C_2 e^{-t/15}$ are correct, but using the information from the graphs we can se that $C_1= -1$ and $C_2= 1$.

From these equations we can see that $r(3)=1-e^{-3}\approx .9502$ and $s(3)= e^{\frac{-1}{5}}\approx .81$ (note that .81 is close enough to 1 for this particular problem). This means that the channel is mostly open as statement 4 asserts.

Now for statement 7 we have $t= 100$ and while $r(100)= 1-e^{-100}\approx1$, and $s(100)=e^{\frac{-100}{15}}\approx 0$. This means the product $r(100)^2* s(100)\approx 1^2 * 0 \approx 0$ thus the channel is mostly closed.

Hope this helps.


Why have ground beetles never evolved the ability to get back up? This may seem like a funny question, but I've seen so many ground beetles upside down on the floor and wondered why they've never evolved the ability to get back up. Wouldn't something like this drastically increase their survivability?

By "floor", I'm assuming you mean a smooth floor like that inside a house or building.  I imagine that these beetles are actually quite good at flipping themselves over when they have something to grab onto -- e.g. a blade of grass, a fallen leaf, etc.  The detritus-free environment that is the modern indoor floor (or smooth path, or paved road) is not part of the natural niche of these organisms, and encountering such surfaces was uncommon in their evolutionary history.  Rare encounters are weak selective forces.


How valid is the theory of human's chimp-pig origin? Edit: I have also asked the question on skeptics.stackexchange.com and it has been answered there. Here is the link.

There is a person called Dr. Eugene McCarthy who has a theory that the origin of humans come from pig-chimp hybridization (online article about his theory). How acceptable is his theory in comparison to the other common theories?

Briefly, the "theory" makes no genetic sense. Pig and human genomes have both been sequenced, and their sequences are completely incompatible with this model.

The "theory" is completely idiotic in many other ways -- debunking it almost becomes difficult because there are so many ways it fails to make sense -- but the genetics alone make it impossible.


High Glucose vs Low Glucose DMEM for Cell Culture I've noticed that in mammalian cell culture, there are often two types of DMEM available. High Glucose and Low Glucose. Does it matter which type I use for culturing of cells (e.g. Hela or HEK293)? Which is the type people normally use?

We typically use High Glucose as cells grow faster.  One caveat is that there are concerns that certain protein modifications (specifically OGlnAc-ylation) may be upregulated in non-physiological (25mM or high glucose) media.


Which cells are responsible for the extracellular matrix remodeling? I am studying a case of tendinopathies induced by an alteration of how the extracellular matrix is being remodeled.

From my understanding there has to be a careful balance of MMP (metallproteinases) and TIMP enzymes to maintain tendon homeostasis.

Which cells produce these enzymes?

Taken from The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease

  Metalloelastase (MMP-12) is (as the name suggests) capable of
  degrading elastin, as well as other extra-cellular matrix components.
  It is produced predominantly by infiltrating macrophages and appears
  essential for macrophage migration through extra-cellular matrix

Matrix Metalloproteinases in Cancer Cell Invasion gives a more thorough description of the various MMP and TIMP types

  MMPs are mainly produced by nonmalignant stromal cells in malignant
  tumors. Tumor cells also secrete factors, such as extracellular MMP
  inducer (EMMPRIN), which enhance the expression of MMPs by stromal
  fibroblasts (see Toole, in this book). In addition, growth factors and
  cytokines secreted by tumor-infiltrating inflammatory cells as well as
  by tumor or stromal cells modulate MMP expression.


Can animals absorb atmospheric sulfur? This is a follow up to this previous question:

In biosynthesis of cysteine and methionine, where does the sulfur come from?

Can animals use gaesous H2S in the atmosphere, say for instance from a sulfur rich hot springs, to aquire sulfur?

No, they can not do this. We don't have the enzymes to metabolize H2S, besides that, it is highly toxic. H2S can be used by some bacteria and archea (so called lithotrophic bacteria), but they are relatively rare.

Sulfur is reduced by plants, which take it up in the form of sulfates and subsequently reduce it to form different sulphur compounds. Animals are dependent on the uptake of sulphur from plant sources, as the sulphur containing amino acids are essential (meaning the cannot be synthesized by themself). The pathway is relatively complex. The image below is from the Wikipedia article on Sulphur assimilation, which I can also recommend, if you want to know all the details.


Why do women mature (physically) earlier than men? All sources I've read (the first page) states that the fact that women mature (in the sense of physical maturing) earlier than man is caused by the earlier selective prunning in brain. Though, this is an explanation just for the mechanism, not for the cause.

So what is the real evolutionary reason women mature earlier (though, probably slower) than men?

This is a question about Neoteny and Heterochrony.

The closest field of study which will have specialists of this kind of topic is the study of the late maturation of humans compared to other species, which has had some research: 5-7 years ago there were some papers measuring the different bone growth rates of humans compared to chimpanzees and exploring the notion of natural selection through preference of immature traits: being attracted to girls with child like faces, smaller nose, large eyes, small voice, babyish, with various causes for example allowing for later brain pruning and longer brain development.

If you research in google publications you can find some research on the topic, for example:

Heterochrony in human evolution: the case for neoteny reconsidered

Sexual selection, physical attractiveness, and facial neoteny: cross-cultural evidence and implications (1995)

The origins of sex differences in human behavior: Evolved dispositions versus social roles.

It's all about evolutionary selection due to survival fitness. A complex age dynamic is at work in human evolution due to our extended lifetime, memory and brain size, amidst heavily variable social patterns (mate selection, monogamy, tribe size, bride rights, patriarchal/matriarchal systems) in paleolithic humans.

Bonobos mature at roughly the same time: 9 years, and female bonobos have a baby at 11 to 13 years. I think that illustrates the flexibility of maturation age according to the role of the adults.

Human females can have babies in between 9 and 15 years for the most part, some of them at 7, so maturation age is an evolutionary trait rapidly changeable according to fitness of the resulting offspring, so it is entirely fine tuned by survival performance.

EDIT: I wrote this answer to be helpful, but apparently my lack of sources and "errors?" deserve a mark down. so here is an additional text:

"They found that Paleolithic girls arrived at menarche - the first occurrence of menstruation - between seven and 13 years. This is a similar age to modern girls, which suggests that this is the evolutionarily determined age of puberty in girls.

'This would have matched the degree of psychosocial maturation necessary to function as an adult in Paleolithic society based on small groups of hunter-gatherers,' they write.

Disease and poor nutrition became more common as humans settled, causing puberty to be delayed. Modern hygiene, nutrition and medicine have allowed the age of menarche to fall to its original range.

However, today there is a mismatch between sexual maturity and psychosocial maturity, with sexual maturity occurring much earlier. This mismatch is a result of society becoming vastly more complex, with psychosocial maturity therefore taking longer to reach."

Note that they are talking about female adult paleolithic maturity and tasks at that age. Females compete for mates by attractiveness and fitness, and some research suggests that males compete for females by other mechanisms, even force or threat.(ref)

There is clearly a reason for which men are available to make and care for their offspring later than females. Females prefer older males by at least a couple of years with moderate adult muscle mass(ref), and in our species males of 17 to 35 years are biologically the strongest and wisest. Nature would have it that 11 /13 year old fathers clearly are counter productive to the survival of their partner and child in an ordinary setting of hunter gatherers, because of the very long gestation and complexity of human survival tasks.

The human mental maturation range has a wide variety of deviation, and between the age of 8 and 25, we are pre-programmed to be in an intense task of learning and physical adventure. Physical coordination of the male can reach an optimal level as late as the age of 22, 3/4 years after his bones have finished growing and his muscles and reflexes have had time to increase and adapt to his new frame, which is why athletes are at their physical peak between the ages of 18-27, and the "mental pruning" article suggests that their mind continues to re-organize itself well beyond the age of 30. During that stage, a human male is programmed to learn a wide array of advanced skills: flint knapping, tool making, botanic knowledge, hunting skills, clothes making, landscape exploration, orientation, memorization of food places, wells, tree climbing, metal work, net weaving, pottery, pigments, weapons, blow darts, wild animal experience (game, lions, rhinos, birds, rodents, traps, stalking, poisons, frogs) etc... All that time based survival experience reinforces the notion that a male reaches his functional optimum as a provider and protector of his family well after his sexual maturation age.

Females have a less physically intensive role to play in human society. While they can learn all the hunting/survival skills of the male, their central role is to be nourished and provide for the child(ref). Their parenting tasks rely less on individual memory because they stay socially at home more (papua new gineans, africans, aborigines, yanomami). Their task can be less intense physically, require less physical training, and can be less intensive on memory and adventure (being nourished, childcare, craftwork, leadership of the group at home and less in exploration and precarious tasks). Both the human male and female memory has a very important role for guiding the group. A female can provide guidance up till the age of 50-90 in a natural setting.

Females are generally less expendable and adventurous than males, because a male can potentially have 3 offspring every day, he is limited by the number of females, and she can only have 1 offspring every 9 months, she is more precious to the multiplication of the group.

Add to that the function of memory, hunter gatherer fitness, and social acumen, absorption of mental and survival skills

Other great apes have gestation periods arount 8.5 months compared to our 9.

Because of the difficulty to assess the paleolithic social and environmental pressures that caused the sex age maturation difference, it's a question that theorists would be unwise to wade into to any great depth, in an academically competetive field. A good anthropologist should be able to list all the predominant selection factors.


Plant identification? Can anyone identify the plant below? It's in a backyard in Pennsylvania, and the photo was taken today.

Those flowers don't come from the same plant as that big leaf in the front do they?  Cant help you with the leaves, but the flower looks like a daylily. source: I know nothing about plants, but happen to have a mom who got a degree in horticulture :)


Is it possible to derive the Michaelis-Menten equation under conditions where the product formation is reversible Text books etc generally derive the Michaelis-Menten equation for the irreversible case i.e $$\ce{E + S <=> ES -> E +P}$$ I can't see how to do it for the reversible case i.e  $$\ce{E + S <=> ES <=> E +P}\;$$ Is it possible?

No it is not possible to derive the equation for the reversible case. This is because the Michaelis-Menten equation is derived on the explicit assumption that the substrate concentration is much greater than the product concentration so that the back reaction does not occur. This is true at the start of a reaction in the lab when you add enzyme to your substrate. At later times when product builds up these conditions no longer hold and the M-M equation breaks down.

It is possible to derive a different equation for the reversible case (as some other posters do) but this begs the question of the importance of the Michaelis-Menten equation for biology. The poster seems to think that it is some universal truth, important in its own right or because it models the reaction in the living cell. I think this misses the point, which I think is as follows.

It originally was a prediction from, and hence a test of, the hypothesis that enzymes have a single active site at which the substrate binds and is converted to products.
It allowed two fundamental aspects of this enzyme model to be quantified: (i) the binding affinity of the substrate for the active site, as the inverse Km, and (ii) the catalytic efficiency ('smartness') as the turnover number or kcat, which is derived from Vmax (and enzyme concentration).
These enzyme constants can be used to address biological questions, for example whether an enzyme capable of a particular reaction in the test tube is able to account for the observed reaction rates in a tissue. Or whether the substrate you find the enzyme can use is likely to be the physiological substrate in a tissue.
It turns up enzymes that do not exhibit M-M kinetics, implying that some aspect of the model does not apply to them. This can be of mainly chemical interest (ping-pong kinetics and the like) or of physiological importance, as in allosteric kinetics (S-shaped rather than hyperbolic curve) shown by multi-subunit enzymes where the individual subunits show co-operativity, allowing more finely tuned regulation.
And if you do want to model reactions within cells, the kinetic constants can be of use. However as one is normally dealing with a chain of reactions in an open system the mathematics are complex (and nothing to do with the equation for a single reversible reaction in the test tube).

Most biochemistry students (and many teachers) would be hard pressed to explain why they should learn the derivation of the Michaelis-Menten equation. The answer is partly so they see that it is based on a particular model of the enzyme, but also so that they are aware of the assumptions on which it is based. Hence they need to be aware that the Michaelis-Menten equation is only true for initial rates of reaction, otherwise their determination of the practically and biologically useful Km and Vmax will be incorrect.


Bright green caterpillar with long white stripes, few hairs, no extensions, possibly Noctuidae Our herbs had strange holes, and we found eight of these caterpillars to be the reason. They were mainly underneath the leafs and measured about 5 cm in length.

We collected them from the herbs, put them in boxes and also fed them (slightly rusty) crisphead lettuce, which they seemed to like just as well.

We tried to identify them, and our best guess was some sort of Noctuidae, possibly Ctenoplusia limbirena. We're located in central Germany.

When disturbed, they froze for several seconds, then slowly began to move (and eat) again. When picked up, they sometimes spit a few drops of green fluid at their attacker.

They ate "a lot" for a few days - and pooped just as much. I cleaned their box twice a day, but as you can see, they were quick to fill it up again. (I hope you don't mind the picture - at least it did not smell at all.)

Now, their behavior changed, and they folded leaves, attaching it with strings to stay in place, and hide in there - I suppose they're about to become pupas.

I would be interested in what species they are, and if they are dangerous to humans. We've always washed hands after contact and avoided touching their poo, though they most viciously attacked my girlfriend's finger with green spit (she survived without any damage).

Further, how can we help them advance to become winged? Is it sufficient to just leave them alone, or should we add more leafs or sticks to their box?

Finally, I was told they would practice cannibalism if food supply were too low - is this true? I would have thought their stomachs are specialized to leaves exclusively.

Edit: Not even a week later, they hatched, and I took some photos before setting them free:

This could be one possibility, two others would be:

Scoliopteryx libatrix (The Herald (moth)), see this image (from here, contains additional information in german):

Orthosia cerasi (Common Quaker) would also fit, see here (from here, contains additional information in german):


Why rectus abdominis is not proximal muscle? I am thinking this picture which shows proximal muscles.

Why for instance pectoralis major, subclavius and rectus abdominalis are not included in proximal muscles?

It's not clear what "proximal" means in this context. It's not a standard use of that anatomical term in English. I'd also say that the figure on the left actually does show the pectoralis major.

The author of this figure might be trying to show the muscles that cross the proximal joints in the upper and lower limbs. For example:

Upper limb

Pectoralis major
Biceps brachii
Triceps brachii
Latissimus dorsi

Lower limb

Adductors (brevis, longus, magnus)
Rectus femoris
Semimembranosus, semitendinosus, biceps femoris (long head)
Gluteals (maximus, medius, minimus)

Muscles that do not cross the shoulder or hip are not included. This explains the lack of rectus abdominis or subclavius. Though it is not clear to me which the paired muscles in the posterior view are running craniocaudally from the thorax to the gluteal region.


What is (are) the medium of conduction for an electrical current with an external source in the human body? I am trying to get some background for some personal research I am doing into the effects of Electro Convulsive Therapy. I don't understand how electric current from an external household source, say, flows through the body. There are no naturally occurring chains of metal atoms in the body, so it can't be electron flow, but my understanding is that the electric field around an electrode is very thin, so I can't see ion flow as accounting for electrical effects in the body at some distance from the electode - particularly with AC, as I would only expect a local oscillation. I am familiar with membrane depolarisation but that is essentially a cellular mechanism - is it (or saltatory conduction) activated by an external current? I know that the body as a whole (and cell membranes in particular) function as a dielectric, but I can't see how this fits into the global picture of current flow between two electrodes. Can anyone help or recommend me a paper?

Electric current flows rather rather easily through water that contains ions, which are electrically charged atoms. Since the human body is more than half water, and that water is filled with ions such as sodium, chlorine, potassium, etc., the body for the most part conducts electricity rather well.  The skin can have a high resistance to the flow of electricity, but it varies substantially, particularly being reduced when the skin is moist.  Medical electrodes, as for heatbeat measurements, are typically applied with conductive paste to overcome most of the skin's resistance.  You may want to look at this "Electricity And Human Body" page, or the article "Conduction of Electrical Current to and Through the Human Body: A Review".


Viability of argon-oxygen atmosphere Can humans breathe an Argon-Oxygen atmosphere, where Argon substitutes the inert Nitrogen gas which currently populates our atmosphere? I didn't quite know which forum to stick this one in; I put it here because I only want to know if such a mixture of gases can be feasibly inhaled, without the prospect of early death by some physiological component.

One may think that Argon, being an inert noble gas, causes no harm at all and can perfectly replace N2 in a mix with oxygen. After all, you've been breathing Argon your whole life, since approximately 1% of the air is Argon:

However, we are talking about a raise from 1% to 78%... and there are possible consequences here:

Argon is way denser than N2: Argon has a density of 1.784 g/L, while N2 has a density of 1.251 g/L (O2 has a density of 1.428 g/l). So, Argon is 40% denser than N2 (and also denser than O2 and denser than air). Without taking into account ventilation and other forces, there is a risk of argon not mixing properly with the incoming "air" in your lungs.
Argon is a narcotic: This may sound strange, but there are evidences that Argon has sedative properties. According to Nowrangi, Tang and Zhang (2014):

  Argon gas is considered a small noble gas element that has been applied in a number of fields. It has been generally classified as a
  nonreactive or inert gas providing a view that it does not contain
  any biologically active characteristics. In fact, argon has
  demonstrated characteristics such as narcosis [...] The mechanism in which argon displays its anesthetic ability has been suggested to be from the stimulation of γ-aminobutyric acid type-A receptors. (emphases mine)

As an additional information, there is an Argon-Oxygen mix, called Argox, which is used for decompression research only, not as a scuba-diving breathing mix.

Also, this question from WorldBuilding has some interesting information (and some wrong information as well).

In conclusion: this Argon-Oxygen mix is not harmless.

Source: Nowrangi, D., Tang, J. and Zhang, J. (2014). Argon gas: a potential neuroprotectant and promising medical therapy. Medical Gas Research, 4(1), p.3.


Could a biological process organically build solid metal "organs"? Human ingenuity has made great use of metal tools. But are there any known, or potential, biological processes that might produce sizable solid metal objects like how for example skeletons and shells are being grown? Does solid metal manufacturing require melting point temperatures beyond what biological processes can survive, or could it be grown by proteins more or less atom by atom?

That is an excellent question. I was a little confused at first because, without realizing it, you actually cited a perfect example of a biological process that manipulates metal: bone formation.

Bone is made of hydroxyapatite crystal, which is a mineral whose main ingredient is, of course, calcium (metal).

Now, to answer the how of your question; bone is formed, as you eluded, through protein to protein interaction mediated by cells called osteoblasts (osteo- = bone, -blast = immature cell). The osteoblast first locates a site on the bone that is to be expanded, then encases itself in a framework of collagen fibers. When this is done, calcium phosphate and hydroxide bind to the collagen and "harden" as hydroxyapatite (Ca10(PO4)6(OH)2). The osteoblast, now encased in a shell of hydroxyapatite (called the lacuna), transforms into an osteocyte (-cyte = mature cell) and projects long arm-like structures called filopodia which it uses as sensors and to communicate with surrounding osteocytes. All that adds up to look an awful lot like this (with respect to the fact that they are usually fully enclosed, but that would make for quite an insipid picture):

Finally, to put Filipe Rocha's concerns to rest, how is this fully organic and (almost) solid metal structure adapted and "unmade," should the need arise? Well, there is a third type of bone cell called an osteoclast (-clast = to break). Osteoclasts break down bone by secreting hydrogen ions to dissolve the calcium in hydroxyapatite, then cathepsin and other protease to digest the collagen network.

So there you go; a fully biological system with the capability to not only create a non-toxic, solid metal structure, but also maintain it and even manipulate and "unmake" it. Even though bone is not an organ, I'm sure this system could be modified for such an implement if we put our minds to it... :)

Edit:
If calcium isn't "metally" enough for you, you might want to check out limpet teeth, which are comprised of goethite, iron oxide-hydroxide (FeO(OH)). I can go further in depth with the biological processes necessary to produce this mineral if you want; just ask. :)


What negative effects can pinhole glasses have on the body? While shopping in the local supermarket yesterday, I was surprised to find this display on one of the shelves.

I also realize that I should have taken a pamphlet with me, as well as a picture of the boxes for the glasses, as seen in the picture to read more about it.

This answer at Skeptics.SE shows that there are in fact probably no long-term benefits of wearing pinhole glasses, but my question is...

What potential harm/side effects can be caused in the short and long-term from wearing this type of eyewear?

Probably not many side effects except in specific instances, but no benefits either. My guess is that there are potential side effects because these glasses reduce the amount of light that the eye receives and restrict the visual field. Therefore, the restricted visual field would be bad for activities such as driving, in which you need your peripheral vision. And the reduced light makes objects appear dimmer, so it is harder to see with them at night. I also imagine (just a guess) that they would be bad for very young infants, who are almost always born without perfect vision and require some visual stimulation to correct.

There are probably many reasons why optometrists use a pinhole occluder for diagnostic purposes, but never prescribe it as treatment...


Definitions of hermaphroditism, dioecious and monoecious? What is the difference between these terms "monoecious","Hermaphrodite".
my lecturer says hermaphrodite is a zoological term and monoecious is botanical term, but in contrary to it, in my textbook both of these terms are used both botany and zoology.

So what is the actual difference?

Below are definitions that I've seen; there may be less strict definitions under which monoecy (the noun form of 'monoecious'). and hermaphroditism would be the same thing.

Dioecious: Although rarely used for animals, one could say that human are dioecious because each individual produces only one type of gamete. In a dioecious species, some individuals are males and others are females.

Monoecious: In monoecious plants, individuals carry both males and female flowers but not flowers that can produce both female and male gametes.

Hermaphrodite: Hermaphroditic plants have flowers that can produce both male and female gametes.

Then, there are many other fancy terms such as dichogamous, gynomonoecious, subandroecious, heterostyly or androgynomonoecious! Plant mating systems are fantastically diverse and complex!

More information

Some of these terms are defined in The Evolution of Sex Determination, which is very pleasant to read. For shorter articles, consider Barrett 2002 or just Wikipedia > plant reproductive morphology or Wikipedia > dioecy (the noun form of 'dioecious').


Can humans shorten their sleeping patterns? Can sleeping patterns be trained, or are they genetic? I read that a human needs to sleep at least 4 hours. Can sleeping time be reduced without having a negative impact?

Polyphasic sleep can allow people to sleep at multiple regular intervals throughout the day and allows people to get by with less total sleep. I don't know of any training that can help people reduce the amount of monophasic sleep they need without a negative impact.


Would a shark whip into a frenzy from smelling its own blood? Sharks normally respond very quickly to the scent of blood in up to a mile radius, but what if the shark itself simply got injured? Would it respond to its own blood at all?

I'm pretty sure, they can smell their own blood, but they do not attack themselves. Wounding a fish results in the release of chemicals into the water. This is a signal for other fish about potential danger and they will escape (Schreckstoff). Of course, the predator of the wounded fish will not mind. So this seems to work best within the same species. Fishermen and military have apparently used dead or rotten sharks in the past to keep sharks from attacking (Shark repellent). I guess, a similar mechanism plays a role here. Sensing a wounded member of the same or close species (including oneself), would block any feeding behavior.

The Myth Busters have actually done this (not very scientific) experiment: https://youtu.be/E1GenfKR9pk


Are we more/less resistant to infectious diseases during an allergic reaction? To my understanding, an allergic response is a non-adaptive response of the immune system to some molecule. The molecule in question is therefore "thought by the immune system" to be infectious although it is not. An allergic response is triggered by immunoglobulin of type E ($IG_E$) and causes an immune reaction.

I'd expect immune responses to not be instataneous, that is I would expect that it takes some time in order for the immune system to achieve some reaction peak. In consequences, I have been wondering whether someone that is under an allergic reaction is more resistant to early development of infectious disease because the immune system is already "switched on" prior to the infection. On the other hand, I would have thought that the body resistance to anything is lowered during an allergic reaction 1) because the allergy diminishes "general health" and 2) because allergic response may kill body cells.

Are we more/less resistant to infectious diseases during an allergic reaction?

There are a number of issues with your question, and the short answer is no.

Immunity to pathogens is conferred by antibodies, but not usually of the IgE group. Pathogens usually stimulate IgM -> IgG; IgAs are present in mucosal surfaces.

There are multiple kinds of "allergic responses", and each carries its own risks.

  Type I reactions (ie, immediate hypersensitivity reactions) involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils.
  Type II reactions (ie, cytotoxic hypersensitivity reactions) involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation.
  Type III reactions (ie, immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation.
  Type IV reactions (ie, delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cells rather than by antibodies.

Limiting ourselves to allergic responses mediated by IgE, we have anaphylaxis, allergic asthma, urticaria, angioedema, allergic rhinitis, some types of drug reactions, and atopic dermatitis. These reactions can result in something as mild as urticaria or as life-threatening as anaphylaxis. None of these conditions carries an increased or decreased general immunological response to pathogens.

If allergy affected immunocompetency, one would expect to see, for example, an increased incidence of fungal infections in allergic individuals, but this is not the case. Allergy does not result in an immunocompromised condition, nor does it result in a primed response (an idea popular in the 90's). They are mediated by different pathways.

Effector mechanisms in allergic reactions
The production of IgE
Allergy, Parasites, and the Hygiene Hypothesis
Immunocompetence and allergy


Do Tardigrades preserve water or replace water? If you find something funny in my argument, then please pardon me, as I lack knowledge of biology. I was reading an article titled as "Water Bears Can Replace All The Fluid In their Bodies With A Glass Matrix"

Being extremely new to biology, I am a bit confused. Do Tardigrades preserve water through this protein or entirely change their biological structure to flush away all the water present in their body and rely on these proteins? Does this mean that their bodies no longer contain water?

Thanks.

neither they are desiccating, some water remains but too little to sustain normal processes, the matrix just preventing all the normally destructive side effects of desiccation that would destroy the cellular machinery, the cellular processes are still essentially stopped.


What kind of mushroom is this in central Europe? I found some mushrooms in the forest and I'd like to know what kind it is, for being able to tell how to protect the trees from it.
Growing Info
growing location: central Europe, forest
host plant: beech tree, alive
season: late Summer (Sept. 15th 2020)
The area where the mushrooms were found is a typical beech forest with unusually low water levels, as the last few summers have been drier and warmer than usual. I presume the trees suffer more from these mushrooms because the trees are weakened due to the hot weather and little rain.
Some of the mushrooms dry out while on the host tree.
Picture Taking Conditions
The closeup pictures were taken at home. This was after transporting the mushrooms and storing them in the fridge for 2 days. They got a bit squeezed during this procedure.
Pictures
host tree:

host tree from below:

multiple mushrooms, pic A:

multiple mushrooms, pic B:

bright mushroom, pic A:

bright mushroom, pic B:

bright mushroom, pic C:

cream colored/older mushroom, pic A:

cream colored/older mushroom, pic B:

cream colored/older mushroom, pic C:

Could be oyster mushroom. Get some books. Look up Pleurotus ostreatus; a book I found it in is primarily for US,although mushrooms often have very wide distribution. One book I have says " The worst thing you can do is pick mushrooms ,then try to decide what they are ;if they are edible". The recommendation is to learn some local editable mushrooms and then hunt for them.


At what substrate concentration will an enzyme work at 40% of its maximum rate if its Km = 0.095M? The question involves the Michaelis-Menten kinetics equation.

Here is what I did: I took the Michaelis-Menten equation, replaced v with 0.4Vmax, canceled the Vmaxes (one on each side), and solved for [S].

I got -0.056 which is obviously wrong, because [S] cannot be negative.

To be honest I know very few about enzymes and absolutely nothing about Michaelis–Menten.

However, when I "took the Michaelis-Menten equation, replaced v with 0.4Vmax, canceled the Vmaxes (one on each side), and solved for [S]", my result is positive:

0.4 * Vmax = S * Vmax / ( Km + S )
0.4 = S / ( Km + S )
S = 0.4 * Km + 0.4 * S
0.6 * S = 0.4 * Km
S = Km * 2 / 3.


Tree identification - Oregon A bit west of Portland. It doesn't look native to me, and we didn't plant it. This is the first year it flowered, so I decided to see if I can get it identified. If it matters, the flowers are aromatic.

This is a Privet (Genus Ligustrum). It appears to be Ligustrum vulgare which is known as Common Privet, or sometimes European Privet.

It is a common woodland understorey shrub in Europe, often planted as garden hedging in urban areas as it is semi-deciduous and responds well to repeated pruning. You could never really call it a tree, it is a shrub species.

The white flowers as you say are quite fragrant and pleasant. They develop into shiny black/dark purple berries.