What is the benefit of near-emptying the bloodstream in the mammalian kidney? In the normal function of the kidney, the bloodstream is near emptied of fluids as it moves through the glomerulus, in which glomerular filtrate is formed.

As it proceeds through the Nephron, a significant amount of this material is returned to the bloodstream, and only a comparatively timy amount goes into the urine.

Why, in evoultionary terms, is it not more favourable energetically to remove only the small number of molecules, perhaph using specialised channels made of protein and activated only by a certain molecules which need removing, at a potentially huge energy saving?

Probably because it's easier to retain what the body wants than get rid of what the body doesn't want.

What does your body want to keep from your Urine? Pretty much water and selective ions (Cl-, K+, Na+, Ca+2, etc.). Maybe a few other things, depending on how healthy you are.

Now, what does your body want to get rid of in your Urine? Well, anything it can't get rid of in your solid waste. That includes pretty much anything water soluble that could harm you, whether it's Urea, chelating agents for heavy metals, ions your body doesn't want (excess minerals), excess vitamins, sugars (to maintain insulin levels), hormones, liver byproducts, and whatever dark horrors mother nature is concocting for us in the forms of virii or whatever else.

That's just the beginning of the list, but already you should start to see the impracticality of having active transport or coupled transport for everything. The list of transmembrane proteins needed to ferry all of the items your body wants to get rid of is a lot longer than the list of transmembrane proteins needed to keep what the body needs.

Then you have the "unknowns" - whatever else your body hasn't encountered yet, but will still be water-soluble. If the body required some sort of transport across membranes for everything it didn't want, then it would need to adapt to every single new compound it encounters. Given the relatively slow generation periods for humans, if a new compound turned out to be significantly fatal then the slow adaptation could spell disaster for any small populations and create serial bottlenecking events.

So, while it may not be energetically favorable to let water and ions pass into the Nephron and subsequent tubules to be reclaimed, Evolutionarily speaking it's probably strongly selected for. We may expend a lot of energy reclaiming water against its concentration gradient, along with whatever else we want from Urine, but at the same time we get rid of everything else we don't need that's filtered through the glomerulus. It doesn't matter what the "everything else" is - but we know we don't need it, and that's the big key.

With my current level of knowledge (B.S. - Biology) this is the best explanation I could think of, but I haven't read any specific papers nor heard any particular theories on why the kidney's components act as they do.


Identify this giant green moth(?) with great taste? One evening in late February I sat down to eat dinner after a day of hiking in hills around New Taipei City and discovered that someone else shared my taste in clothes. A very large green moth-like insect had landed on my pants with a green floral pattern. The inset in the first photo shows that the body was about 5.5 centimeters long. Included are additional cropped top, side and front photos, the top one without flash for a better appreciation of the colors.

It frightened me at first because it was just sitting there and I have no idea how long I'd been walking around with it. After it's photo shoot I brought it outside and located some bushes and was able to convince it to move. It seemed quite sluggish though it wasn't very cool yet (I estimate perhaps 22 C)

Can anyone identify this obviously style-conscious insect, and speculate why it was lethargic and not interested in flying away?

That appears to be an Oleander Hawk-moth a member of the Sphinx moth family.

I think the only other possibility for Taiwan is the quite similar Jade Hawk-moth, but that supposedly has a dark purplish colored head.

Image for comparison:

Source: Shantanu Kuveskar / CC BY-SA.


What are the known energy capturing processes in biological systems? I am not a biologist. I am aware that photosynthesis is the main process for capturing electromagnetic energy from the Sun. Also, I am aware that some bacteria can capture energy from boiling water and others from certain chemicals.

What are the known energy capturing processes in biological systems other than photosynthesis? I am looking for references or a good survey of all known mechanisms.
Is there an explanation for the ingenuity of evolution in solving the energy capturing (transforming) problem via multitude of mechanisms?

Apart from phototrophy, there is only chemotrophy (obtaining energy from redox reactions of chemical substances) and radiotrophy (obtaining energy from ionizing radiation such as gamma rays). However, radiotrophy as of now is only known to be a supplemental mode of energy and not a primary one.
Diversity is a central theme of evolution. It would be interesting if there was a single common mechanism for all modes of energy-nutrition which is perhaps true for the case of the chemiosmotic energy generating mechanism (ATP-synthase like systems which generate energy from chemical gradients). Otherwise, diversity is expected as the organisms evolve to survive in different environments.


What is happening to this spider? I was trailing through a local bird sanctuary yesterday (central Kentucky, USA) and came across this spider.. it's definitely dead, but what is hanging from the back part of its abdomen? Has some parasite taken home within it, and that is its "nest"?

It is hard to say for certain, but the insect hanging from the spider looks like it may be a member of the family Elateridae, commonly known as a "click beetle". As far as I know, they're harmless and no threat to a spider.

The close binding of the legs with silk suggest that the click beetle(if that is indeed what the insect is) may have been a meal prior to the spider's death, or packaged for later consumption.

Given the amount of debris in the webbing surrounding the spider's corpse, including some pieces of some sort of grass leaves, it seems likely that the webbing become tangled during or after the spider's death.  The placement of the click beetle is likely coincidental, although I suppose it is possible, given the positioning, the size of the click beetle, and what we can conjecture would be the size of the wound if that black material is seepage from a wound on the spider's abdomen, that some force actually punctured the spider's abdomen with the body of the click beetle.


BLAST DNA Sequences Reversed I have been trying to learn some basic DNA sequencing techniques and have been using BLAST as a reference. I thought that I was starting to get it, but then I cam across this:

It looks like it's saying that the match starts at 10835 and ends at a smaller index (10714).
I tried clicking the link to view the full sequence, and I couldn't find the highlighted portion anywhere (not at 10835 or at 10776).

My question is: Where (in NR_046235.1) can I find the highlighted sequence?
And what does it mean to say that the Sbjct starts at 10835 and ends at a lower index?

I can post my query if necessary.
Thanks.

Note that the query sequence you have provided matches the minus strand of your target sequence. That means not only that the target sequence will be reversed (as you have noted), but it will also be complemented as well. So in the GenBank record, you should not look for the sequence CCGACCGA... starting at position 10835, you should look for the sequence ...TCGGTCGG ending at 10835.

ccgaccga...    minus strand
||||||||
bbɔʇbbɔʇ...    forward strand

The sequence in the GenBank record contains spaces, so that complicates finding your sequence using the browser's "Find" function, but if you use the position indices at the beginning and end of each line of sequence, you will be able to find the reverse complement of the matched sequence reported in the BLAST results.


How does RNA polymerase achieve higher processivity? DNA polymerase uses a sliding clamp in order to replicate DNA. RNA polymerase does not require one. What allows RNA polymerase to hold on to DNA just like DNA polymerase?

The structure in the presence of s (holoenzyme) is on the right; note the open channel for DNA binding. The structure in the absence of s (the core enzyme) is on the left.  Note that the channel is now closed, as if the fingers and thumbs of a hand now closed to make a circle. This striking conformational change that occurs when s dissociates is thought to confer high processivity on the RNA polymerase.

SOURCE: http://biowiki.ucdavis.edu/Genetics/Unit_III%3A_The_Pathway_of_Gene_Expression/10%3A_Transcription%3A_RNA_polymerases


Why introduction of an extra copy of a gene related to pigmentation causes RNA interference in Petunia? RNAi became famous after Fire and Mello experiment in C.elegans; however, it had been observed before. In the 80's, Jorgensen was trying to increase pigmentation of Petunia flowers by introducing extra copies of chalcone synthetase gene, which encodes an enzyme involved in anthocyanin synthesis.

However, this experiment lead to post transcriptional gene silencing (PTGS) by a mechanism that was not understood at that time, called RNA interference.

Here
you might find more information about the experiment (including the vector used to introduce the gene).

I know how RNAi works by the classical pathway; however, I didn't understand how an extra copy of the gene could generate gene silencing. Introducing of DNA sequences has been used to knock downs target genes, however, generally these sequences are planned so that they will form a hairpin which is recognised by Dicer; probably, the researcher did not use such a sequence. Moreover, exogenenic genes are widely used without resulting in unplanned RNAi.

Does someone know more information about what possibly happened in the experiment to produce RNAi?

The answer is in the slides you provided a link to. The key fact is that Craig & Andy did careful controls to show that it was the presence of dsRNA in both the sense control, and in the anti-sense experimental sample that was responsible for the RNAi-mediated knock-down.  Actually, Ken Kemphues showed this earlier in a Nature paper (the control also knocked down gene expression) but did not pursue the mechanism.

Therefore, I infer that the transgenic gene expression construct introduced into the petunias must also give rise to dsRNA. I am less familiar with the consequences of introducing foreign DNA into a plant cell (e.g., does a single copy become integrated, multiple copies?, is it maintained extrachromosomally?)


If humans had cellulase would they be able to digest grass? Cellulase is an enzyme capable of breaking cellulose. If humans were able to produce cellulase in our stomach would we be able to digest grass? If not, what more things would we need in order to digest grass?

No. Even for an herbivore, digesting grass, or plants to be more general, is hard, because they contain cellulose. Herbivores have different parts of a stomach, whereas humans only have one compartment, so in herbivores, the plants (or grass) enter the first part of their stomachs called the rumen, which contains a salty solution that breaks down cellulose, then, the herbivore will regurgitate the processed food, or cud, from the rumen, into their mouths, and break down the cellulose even MORE. The cud then enters back into the rumen and then digests as normal. So even if a human had cellulase, they would need a rumen, to break down the cellulose further.


Please help me to identify this red worm I found bunch of red worms coming out of sink.
It is rather unusual to find an overwhelmingly large number of worms. It doesn't seem like earthworm or horsehair worm. I don't know much about the worms though.

Could anyone please identify it for me.?  Notable features are

Dark red in color.
Has  a hook like structure at its rear end.
Moves in both directions front and rear.
It shrinks when it dwells in water.

Judging from the photo, it's an earthworm, some species of Lumbricidae. If the accident happened in India, this faunistic paper can be of some help.


Human body power consumption in still state I'd like to know what kind of power human body needs to maintain life, in still state (average daily power consumption of an average man is also of interest). In terms of watts.

I've only managed to find one figure - 1700 kcal per day without physical activity. That converts to 80 watts, which seems (intuitively) a bit low, so I wonder if it's the right figure or not.

You're basically correct.  I don't know if you've found the Wikipedia article on Basal Metabolic Rate but it's got everything you need, including a bunch of formulas you can use to figure out an average value for a given body type.  There are also many online calculators, such as this one.  You can easily figure out averages, which I think is what you want, but between two individuals the number can change quite a bit.

Why does 80 watts sound so low?  This is more of a physics.se answer, but Watts are a unit of power which mean they measure energy use over time; W=J/s, or Joules per second.  Every second.  Have you ever touched a 75 watt lightbulb?  They're hot as hell.  If your human does nothing all day, s/he will be like an inefficient incandescent lightbulb on for a full 24 hours.  Maybe that seems low but electricity is relatively cheap these days.  To use another classic physics experiment, 1700kcal=7000kJ=a lot of ice turned into steam.

No wonder my father always made me turn the light off in the bathroom...


Argentine Ant Trails What is the maximum distance for an argentine ant (Linepithema humile) trail?  I imagine that there is some point where the ants are unable to make the return trip either through exhaustion or from the chemicals of the trail failing somehow.

I was reading "Adventures among Ants", by Mark Moffett, to see if he said something about the length of the trails of Argentine ants and I was about to give up and give a general answer based on the other information about Argentine ants in the book, when I hit upon this quote by "Physicist turned biologist Jean-louis Deneubourg":

  The Argentine ants' exploratory behavior is exceptional in that they mark continually and explore collectively. Whereas other recruitment trails are constructed between two points (e.g., nest and food), their exploratory trails have no known destination, progressively advancing into the unknown. They rapidly lead new explorers to the frontier between the just explored and the about to be explored zones, avoiding situations where ants will end up exploring the same zone twice, and help returning explorers reach the next directly. A wide corridor of the chemically unmarked area is thus systematically "swept' and marked in a minimum time with maximum economy.

The things to know about Argentine ants are, they form supercolonies in which all ants from the same supercolony can mingle indifferently, regardless of the nest they are from. There is no theoretical limit on the size of such a supercolony; if there is one, it is over thousands of kilometers:

  The largest [Argentine ant supercolony] extends from Italy to Spain's Atlantic coast, a distance approaching 2,000 kilometers

This means that the length of an Argentine ant trail is definitely not limited by ant exhaustion or chemical evaporation, depending on what we mean by "trail". If interconnected trails can be counted as a single one you could theoretically have a 2000-km Argentine ant trail that is maintained by ants all along its length. In practice the trail lengths are probably still limited, but by their purpose instead of hard physical limitations. The Deneubourg quote says recruitment trails are built between two specific points, such as a nest and food: this example clearly implies a distance limited by nest density (the trail between a nest and food will be from the nest closest to the food, so if nests are all 10m apart the length of the trail will be 5m at most). This would be true of any trail that has a nest as an endpoint, and what other kind are there?

He also says exploratory trails have no fixed destination, but that doesn't mean they cover unlimited distance either: the exploratory front as described clearly moves forward gradually and deliberately, and as Argentine ants are constantly building nests within the territory of the colony, the exploration front will always be a certain limited distance from the nearest nest.

Then again we could also argue that nest density is itself determined by a physical limit on maximum trail length, which could indeed be ant exhaustion (or ant loss of efficiency at least), risk of the trail being perturbed, chemical evaporation (as in, a longer trail would need more ants to maintain it), etc. I can't speak to that.

Trying to find numbers on Argentine ant nest density I fell upon this paper, which gives more information about ant colony structure and gives the closest thing I think you will find to a definite answer to your question:

Nest connectivity and colony structure in unicolonial Argentine ants

  In experiments using labeled food, and in a 3-year census of nests and trails, we found that food was shared and nests were linked by trails at distances up to 50 meters.

Note that this is "path distance", i.e. the length of interconnected sets of trails. I couldn't find statements on a single trail, but they show a figure and the longest trail on it is between nests that are about 12m apart.

As an aside, this very interesting paper breaks up the "supercolony" concept a bit; while supercolonies are defined by seeing which ants will attack one another, meaning you can legitimately drop an ant from one end of the colony into the other end and it will go to work unmolested as if it were home, the authors of this paper looked at actual worker movement and food sharing, and found that

  Argentine ant populations do not function ecologically as single, large supercolonies, but instead as mosaics of smaller, distinct colonies consisting of groups of interacting nests.

It also says the distribution pattern of nests is seasonal (Argentine ants have very ephemeral nests to begin with); this could give some clue as to what determines nest density and whether physical limits on trail length play a role.


Determining how much energy a plant takes in? I asked a question on WorldBuilding.SE, "Are diamond berries possible?".

This led to asking a question on Chemistry.SE about the amount of energy required to burn a 1 ct. diamond (−6.527kJ).

The helpful commenter on WB.SE said that a plant would roughly require three times this amount of energy to essentially reverse the process through some biological means to create the diamond berry.  And that I would need to know the "wattage input" of various plants to compare with my hypothetical plant.

Is there a way to arrive at how much energy various plants take in?

Also any other related information from a biological perspective would be helpful.

Just a speculation for whether diamond berries could exist or not. This is not an answer for "what is the energy uptake rate of plants" because the actual question tends to be "whether a plant can gather enough energy to form diamonds". For energy uptake rate of plants please see MCM's answer.

Even though enthalpy of formation is same as heat required for destruction, burning a diamond is much easier than creating it (I presume it is easier to generate high temperature compared to high pressure). Natural diamond requires both high pressure and temperature to form. Synthetic diamonds are made by chemical vapour deposition; that also requires high temperature. Such high energies cannot be produced by any known organism (requires devices like arc furnace), and moreover at these temperatures the biological structure will disintegrate.

However there is one possibility of diamond berries; the berries would not be solid diamond though. A plant could be growing in an area where there are a lot of nanodiamonds (meteorite rocks) which could be bioaccumulated in the berries. Living organisms do accumulate nanoparticles [1,2]. There have been studies on biological application and effects of nanodiamonds too [3,4]. However these would not look lustrous like bigger diamonds. Xylem vessels in trees have a mean diameter of 30-40µm; it may be possible that the plant can take up bigger sized diamond particles. Density of diamond is ~3g/cm3 — three times that of water and it would require thrice the force required for water to get diamond to the destination.

For a spherical diamond of diameter 20µm:

Cross sectional Area = 314.15 µm2
Volume = 3351 µm3
Mass = 3×3351×10-12 ≅ 10-8 g
Gravitational force on the diamond = 9.8×10-8 ≅ 10-7 N
Pressure required to counteract gravity = 10-7/314.15×10-12 ≅ 3.18×102 Pa

However, I am not sure if that much of pressure can be generated within a vessel and whether small particles can be lifted like this.

There is another possibility that bigger diamonds are encapsulated by living tissue (not the fruits of course).


Are there any animal species other than humans & chimps that engage in tribal conflicts? i.e., between tribes within the specie.

(For chimps, see, e.g., https://news.nationalgeographic.com/2016/01/160130-animals-insects-ants-war-chimpanzees-science.)

Am seeking examples to develop taxonomy of such conflicts, e.g., for resource acquisition, enslavement, etc.

In the introduction of an article by Gavrilets and Fortunato, the authors give (with references) some examples of intra-specific group conflicts:

  Social organisms living in stable groups often engage in aggressive interactions with conspecifics from neighbouring groups over territory, mating opportunities and other resources... Examples include border patrols in chimpanzees, raiding parties in spider monkeys, clan wars in hyenas and between-group fights in lions, free-ranging dogs, meerkats, Capuchin monkeys, blue monkeys, black howler monkeys and ring-tail lemurs.

Whether these conflicts (or others, such as ant colony conflicts) meet your definition of "tribal conflicts" you will have to decide.


Barring Antibody-dependent enhancement (ADE), how else can vaccines enhance the infection? The link to the 2007 article below was broken for me. I Googled and read it on NCBI.

  Decades ago, vaccines developed against another coronavirus, feline infectious peritonitis virus, increased cats’ risk of developing the disease caused by the virus (T. Takano et al. J. Vet. Med. Sci. 81, 911–915; 2019). Similar phenomena have been seen in animal studies for other viruses, including the coronavirus that causes SARS (Y. W. Kam et al. Vaccine 25, 729–740; 2007).

At p 737 on the right column, the authors "could exclude this mechanism of enhancement as
sera from triSpike vaccinated mice did neutralize, rather
than enhance, virus infection on VeroE6 cells." So I similarly exclude ADE for this question. But in the last para. they wrote

  Interestingly, we observed the
  enhancement phenotype only in human B cell lines but not in
  mouse macrophages despite the presence of FcγRII. Reasons
  for this are unclear, but the respective role of activating and
  inhibiting human FcγRII which have identical extracellular

p. 738

  but heterologous intracellular domains and signaling capacities
  might play a role [63].

Vaccines are now well-tested to make sure that they don't do make infection worse, but there are many ways they COULD.

Two early formalin-inactivated vaccines (RSV and measles) both had this effect. See this Reddit post  to understand the mechanisms.

Theoretically, a poorly-designed vaccine could worsen viral infections  in three ways:

by biasing the adaptive immune response in the wrong direction that makes it harder to effectively respond to the actual virus.  This might be by priming the wrong type of response, e.g. producing a strongly biased Th2 response when a Th1 is required); creating the right response but to the wrong epitopes, in a way that subsequent exposures can't overcome - "original antigenic sin"; or by inducing T/B cell anergy or tolerance to the virus in question.
immunopathology.  For many viruses, the immune system's attempts to kill the virus, not the virus itself's direct cytolytic effects, damage the host.  E,g, Hepatitis C has 3 broad outcomes to a natural infection:  about 20% of people create an early, strong, multi-specific CD4/8 response that clears the virus.  The rest develop chronic infection.  In most people with chronic infection, the immune response damages little - viral loads can be extremely high but liver fibrosis is minimal.  But in \~10-20%, there is a strong immune response: chronic inflammation, infiltration of lymphocytes, and constant direct killing of virally-infected hepatocytes by CTLs leads to deposition of scar tissue and, eventually, cirrhosis.  So if you created a vaccine that failed to clear the virus and instead generated a pro-inflammatory, pro-fibrotic immune response, it would be a disaster.
Increased target cells.  This was a concern with one of the experimental HIV vaccines.  It increased the number of CD4+ cells permissive to HIV infection in the female genital tract (and the rectum, but I don't remember), thus giving the virus more target cells to infect (there was also an experimental HPV vaccine that was feared to do the same).  Those vaccinated thus had increased risk of infection.


identification of this flower I saw this flower in Pulau Ubin in Singapore. Can anyone identify the species of this flower?

It is indeed the Nerium oleander.. For more info refer to this link and also this


How many human cells are there in our body, on average? How many human cells are there in our body, on average?

Wikipedia says 1013:

  Bacterial cells are much smaller than human cells, and there are at least ten times as many bacteria as human cells in the body (approximately 1014 versus 1013).

The Nobel site says 1014:

  An adult human being has approximately 100 000 billion cells, all originating from a single cell, the fertilized egg cell.

The Physics fact book insists it's 1013:

  (length of 1 bp)(number of bp per cell)(number of cells in the body)
  (0.34 × 10-9 m)(6 × 109)(1013)

Finally, Wolfram Alpha gives 1.0 × 1014 as fact:

  Estimated number of eukaryotic (human) cells in the human body: 1.0×1014

I am quite confused: who is right here?

Bianconi et al. 2013 give an estimated lower bound of 3.72 × 10^13 (which, by the way, is approximately the geometric mean of 10^13 and 10^14).

However, from the table in their Supplemental Information (where estimates for about fifty different types of cells are added up), it is clear that the vast majority of these are the erythrocytes, also known as red blood cells: estimated at 2.63 × 10^13. While the second largest class are the glial cells (from the nervous system), estimated at 0.30 × 10^13. Three other classes (endothelial cells {vessels}, dermal fibroblasts {skin}, and platelets {blood}) add up to another 0.58 × 10^13. These, in total, is about 3.5 × 10^13, and we can stop there, because the uncertainty in all these estimates swamps all the other cell type populations, which are much smaller.

This means that if we only consider the 5 most abundant cell types in the body, we already get a very good estimate. Is it likely that we have missed a cell type of which there are a trillion cells in the body? It's not impossible, but unlikely, because it would be hard to miss all these cells.

Maybe there is a long tail (i.e. a large number of minor cell types, each with a small, but significant population) that wasn't considered? Together, these could add up to a significant adjustment to the above figure. I don't know.

This estimate is for a typical human person: 30 year old young adult, 70 kg, 1.72 m tall and with a surface area of 1.85 m^2. For this person, the figure is given with roughly a +-20% uncertainty.

Given all the above, it's probably safe to say "30 to 50 trillion".

(This obviously doesn't take into account any of the bacteria mentioned above.)


molecular indicators of apoptosis: clarification needed I understand that DNA fragmentation is a molecular indicator of apoptosis. What distinguishes this as a hallmark of programmed cell death, versus one of necrosis?

Although both involve DNA fragmentation, the pattern produced is very different.  During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern.  Necrosis, on the other hand, is a more stochastic process, and will produce a smear.  This details the difference rather nicely, including different ways to assay for either one in table 18.3.1 such as morphological staining or flow cytometry.

Here's a nifty image from the link.  Figure 18.3.2.  M is the marker, and in panel A, a conventional gel, lane 1 is apoptotic DNA, lane 2 is unprocessed DNA, and lane 3 is necrotic DNA.  In panel B, a pulsed-field gel, lanes 1 2 and 3 are untreated, apoptotic, and necrotic, respectively.


Energy transfer from P680 to oxygen-evolving complex This topic is confusing me.

As I understand it, in the PS2, photons are used to split water into molecular oxygen + protons and electrons in the oxygen-evolving complex. To do this, a photon is used to excite an electron in the P680, this electron is then released to go through the electron transport chain and somehow the oxygen-evolving complex gets energy from it to make water endure a "photochemical reaction" as described in my biology book.

But how the electron can transfer its energy to the oxygen-evolving complex if it went directly to the electron transport chain? how the energy produced in the P680 transported to the Oxygen-evolving complex?

I would appreciate simple terms as I'm still a college student.

You have to think the other way around: don't pay attention to where the electron from P680 is going.

Instead of that, pay attention to this fact: after PSII absorbs a photon and triggers the loss of an electron from a P680 chlorophyll a molecule, this P680 has now an electron deficit. That is, this P680 has lost one electron.

This P680 without one electron is now called P680+. And here comes the important information, which answers your question: According to Lodish (2002),

  P680+, the photochemically oxidized reaction-center chlorophyll of PSII, is the strongest biological oxidant known. (emphasis mine)

And that explains what (thermodynamically) drives O2-evolving complex (still according to Lodish, 2002):

  The reduction potential of P680+ is more positive than that of water, and thus it can oxidize water to give O2 and H+ ions. (emphasis mine)

I hope those terms are simple enough for you. Finally, for better understanding all this, have a look at the concept of reduction potential (which, as a college student, I believe you have to study).

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman.


What are the sources of energy that alcohol provides? Milk contains sugar and proteins which give energy. What compounds in alcoholic beverages (edited) give energy? Are they more likely to turn into fat (as in beer belly) than blood glucose?

Ethanol is converted into AcKoA, which can be "burned" in the Krebs cycle or can be used to build fatty acids.

By chronic alcohol consumption there is another pathway involving MEOS which converts ethanol to AcKoA as well.

  Are they more likely to turn into fat (as in beer belly) than blood
  glucose?

It won't turn into glucose, just into fat.

Note:

It is suspected that in extreme cases, like low glucose diets and starvation there is an AcKoA -> glucose pathway.

2011 - In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans

So in theory it is possible to convert ethanol to glucose, but there is not enough evidence of that yet. Normally this conversion (if it exists) does not happen, or it has a very low rate...

  What compounds in alcoholic beverages (edited) give energy?

Mostly ethanol and sugar. E.g. sweet wine contains a lot of sugar, not just ethanol...


Lack of A/B-antigen equivalent to Rhesus disease Rhesus disease occurs when an Rh- mother is exposed to Rh antigens (often due to blood contact with an Rh+ child during delivery) and mounts an immune response which eventually results in the production of IgG Rh antibodies. In subsequent pregnancies, these antibodies cross the placenta. When the foetus is Rh+, these antibodies can bind to the corresponding antigens on the foetal erythrocytes and cause haemolysis, which can result in anaemia or even, in serious cases, stillbirth.

Given all of this, why does the same principle not apply to A and B antibodies? In other words, what is special about Rhesus antigens or antibodies that does not apply to other erythrocytic antigens or their corresponding antibodies?

I'm specifically wondering about Rhesus disease and its effects on the foetus, and why similar effects do not occur on the foetus in the case of an ABO type mismatch between mother and foetus.

So it turns out it can occur. It's called Hemolytic Disease of the Newborn (ABO), and according to the article (the relevant citations are a book and some journals to which I do not have access), it is very rare, and severe cases are even more rare. Apparently anti-A and anti-B antibodies are typically of the IgM isotype, which cannot cross the placental barrier. However, occasionally IgG is produced, which can cross.

This is what causes the hemolysis in the fetus - if the mother is type O, and the baby is either A or B, the mother is exposed to unknown antigen and produces antibodies. If they happen to class-switch to IgG, they can cross the placenta and, if in large enough quantities, cause the opsonization and lysis of red blood cells.


Why insects are attracted towards light? Many insects like bees, dragonflies, wasps and other small insects are attracted towards light. Sometimes they are in groups, sometimes they are in solitude. When the light source source is switched off, they do not fly, rather stay still. What causes them to be so attracted towards light?

Phototaxis is a common behavior to many species, including insects but not only (e.g. most fishes do phototaxis).

The ethological reason is quite simple: with light you can see, and if you see you can find food, avoid predators and increase your survival chances. Phototaxis is thus a very strong innate reflex: at the neural scale in many species it is "hardwired".

I would say that the initial "purpose" of this reflex was to avoid shade areas during daytime, the light during nightime being pretty rare before man invented artificial light. The fact that insects gather around artificial lights during nightime is, to me, a side effect of this reflex.


Why does plucking nose hair cause tears in the eyes? It's not a particularly sad or painful thing to pluck a few nose hairs, but it's common for the tear ducts to wet up when doing this.

I would like to know the physiological reason for the correlation, how/why are the tear ducts and nose hairs related in the human body?

Also, tears are an intrinsic pain response and considering the dermal-derivative nature of hair, there are loose nerve endings ensnaring the follicular area, so the sensory neurons detect pain and tears are a physical manifestation of the pain, cuing the body to avoid that stimulus again.


Why did mammals evolve to have two testes? What makes mammals tend to evolve to have two testes?

EvoDevo is not my field, but I will try to give you some pointers.

Mammals as vertebrates, start out as fertilized oocytes, transform into a rapidly dividing lump of cells with eventual polarity through numerous gradients of numerous chemical messengers, and form a neural tube.
The forming body is ever more segmented through the use of gradients and thresholds (see french flag model) and (dorsoventral) axial symmetry is maintained throughout development, and as such two testes represent the default development.

Therefore, it may be more interesting to ask for singular organs which require more information, and thus maintenance throughout evolution of this information. But when considering the energy requirements, the need for synchronization, the need for a separate blood supply and thus the introduction of additional faults, it is easy to see why we only have one heart.

Wikipedia; author: Zephyris, title: "The first few weeks of embryogenesis in humans", DOR: 25/09/2012

See:

Inversion
Evolutionary developmental biology

I hope this helps as a starting point.


Why do only humans commit suicide? Why is it that only humans commit suicide?

Many animals do 'brave' things to protect their children or family, and some male spiders sacrifice themselves so that they can impregnate the females. However, humans commit suicide without necessarily any intention to help their offspring. Why?

Animals can hurt themselves to save their life for example foxes and tigers falling in traps are known to chew their paws to escape from the trap. Thus one can argue that all living creatures want to live and to escape death as well as losing freedom.

looking at how animals live, an animal can always use its capabilities to escape danger or problems as well as to look for food for survival. In humans who commit suicide sometimes it is because  there is no "exit". for example some people commit suicide due to being unable to pay their loans it is the feeling of distress losing all hope and the fact that it is hard to escape from problems in a human society that lead to this thinking.

so a person doing so is trying to escape the problems instead of facing them. further, the fact that humans have the concept of "responsibility" and being held accountable by members of the society all these lead to this thinking as the only escape


What causes people to smell one persistent smell during Covid-19 infection? Some of the people I know got COVID and they loss the smell. After discussing with them about it, they told me that they only smell one persistent smell, everywhere (like onion). Is this frequent for people with loss of smell ? How this is possible ?

At this time any hypothesis regarding the parosmia seems to be untested.  Speculative sentences in lay and technical sources point toward the olfactory bulb.  (I have seen indications regarding the cilia of the olfactory neurons, the bulb itself, and the blood supply, but this seems to stray from our topic)
When we look in more detail, the olfactory bulb consists largely of glomeruli (balls of neuropil about 0.1-0.2 mm in size), which receive input from specific kinds of olfactory neurons that receive from specific odorant receptors (ORs).  See this figure for the situation in mice.  The dorsal region of the olfactory bulb is mostly one type of these, Class I ORs, and the ventral part is all Class II. (more)  If you are following this research you might want to try to figure out if the odors people report are mostly Class I (more hydrophilic) or Class II (more hydrophobic), which might allow you to hypothesize something about the relative strengths of signals from these regions in the model you develop.  Reading anecdotes is scientifically useless, but fascinating - this man describes citrus as tasting "extremely oxidized", which certainly fuels a speculation along that line.
Answering the question in any good way would seem to demand good human olfactory tissue from people who catch Covid, suffer ongoing parosmia, die from something else, and then donate their brains to science.  I'm not sure we're going to see a definitive answer that way soon.  It would be worth keeping an eye out for fMRI data.  I suspect that well-focused high-frequency terahertz might be used to image or even stimulate olfactory glomeruli (phones with 'smell-o-vision') but for now that's science fiction.


Saturated Mutagenesis Screening I am hoping to mutate the active site of the enzyme I am researching that has 5 residues in proximity with the substrate. I am wondering how many colonies I'll have to assess to theoretically sample all the possible mutant combinations?
I am guessing that just screening the number of possible combinations will not be very successful because I am likely to sample a particular mutant more than once?
I have been looking at 'NNK Saturated Mutagenesis' which uses the redundancy in the genetic code to be able to create all residue encodings where N = A/G/C/T and K = G/T, while limiting the number of repeated residues from synonymous codons.
Are there any other ways of performing this sort of mutagenesis with better codon compression?

This sort of method is indeed quite useful and frequently used in synthetic biology: I've used a similar approach before to generate 5' insulators for promoters.
Calculating the exact theoretical likelihood of what you want, so far as I understand, is a complex combinatoric equation that I wasn't able to get a nice closed form on with a few minutes of work. For your purposes, however, I expect that a reasonable estimate will do as well, and that can be made much more easily by modeling the population of each combination as an independent series of biased coin flips, i.e., a binomial distribution.
Consider a situation with $n$ potential combinations that you attempt to cover with $k$ random mutants. If we focus on a particular combination, we can see that each random mutant has a $\frac{1}{n}$ chance of hitting that combination. The whole set of mutants is thus a series of $k$ biased coin flips, with a probability $p_0 = (1-\frac{1}{n})^k$ of getting no mutants that hit that combination. This means that the probability $p_c$ that the combination is covered is $p_c = 1-p_0$, expanding to: $$p_c = 1-(1-\frac{1}{n})^k$$
With a large number of potential combinations and a large number of mutants, we can make a reasonable approximate by treating each combination as independent. In this case, the probability that all combinations are covered is the product of the probabilities that each combination is covered independently. They aren't actually independent: each combination that gets covered slightly detracts from the ability of other combinations to be covered. An estimate using an independence assumption is thus an overestimate of the actual likelihood, and the higher that $k$ is the closer the estimate should be to the exact probability. In short:
$$p_{all} < (1-(1-\frac{1}{n})^k)^n$$
This smells like the sort of equation there ought to be a nice identity for, but I don't know the identity, so I'll just give a couple of examples of calculating with it:

NNK = 32 combinations, 50 mutants (n=32, k=50): $p_{all}$ < 0.07%
NNK = 32 combinations, 100 mutants (n=32, k=100): $p_{all}$ < 25.5%
NNK = 32 combinations, 200 mutants (n=32, k=200): $p_{all}$ < 94.6%

As you can see there's a sharp transition as the coverage count increases.
Important caveat: the theoretical value may not give you what you want. In the paper I linked above, we used two degenerate primers with 18 N bases to inject 36bp of random material, which means we had $4.7x10^{21}$ possible combinations and should never have seen a repeat --- except that sequencing showed that we did indeed get several repeats out of only a few hundred colonies. Thus, biases in the biology may lead your statistics to be skewed from what the theory suggests.


What is the counter-reponse to a sound stimulus? I am slightly confused on finding out what is the counter-response because of a stimulus.

For example, if we hear a sound, I believe the sound waves are the stimuli? So is the counter-response the vibration of our eardrum or the sensation of hearing the sound?

All stimuli do not generate reactions. It is the CNS that decides if a reaction has to be generated on receiving the information about a stimulus.

  External stimuli are capable of producing systemic responses throughout the body, as in the fight-or-flight response. In order for a stimulus to be detected with high probability, its level must exceed the absolute threshold; if a signal does reach threshold, the information is transmitted to the central nervous system (CNS), where it is integrated and a decision on how to react is made. Although stimuli commonly cause the body to respond, it is the CNS that finally determines whether a signal causes a reaction or not.

From Wikipedia

The changes that occur inside ear,vibration of tympanum, movement of ear ossicles and all are responses to the stimulus (the mentioned two are mechanical responses) to transmit the information about the stimulus(sound) to the brain.

If the brain finds out that the sound is actually a noise then it would instruct the body (limbs for example) to move away from the source of the sound. This is then called the reaction.

If the sound is not that loud, i.e. not potentially damaging to the ears then the CNS does not instruct to retreat.


Designing degenerate primers using alignment of protein sequences from other species I am trying to design a PCR primer for a gene whose sequence is not known. Even the whole transcriptome sequencing done in our lab did not identify that particular gene. Hence, I guess I am left with only one option: to design the degenerate primers for this gene by performing sequence alignment of the given protein from several related species and designing primers based on conserved region. Could you please explain the process of primer design by this method. I know some steps which I have described below stepwise:

step 1: download sequence of protein in question from related species from NCBI in FASTA format

step 2: perform alignment using clustal omega

step 3: identify the conserved domains

I am not sure how to move forward from here. I tried J-codehop for next steps but it is asking many parameters for which I have no clue.
Thanks

Try going through this tutorial: http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
It is a nice introduction on how to use multiseq and identify conserved domains from AA or nt sequences across many taxa.

Also check out http://fungene.cme.msu.edu/
The RDP staff at Michigan State University are the masters of doing exactly what you're trying to do.


Any idea what plant is this? I was asked by my biology teacher to find out it’s name but it seems like a pretty common plant to me so I have no idea how to start. Any idea what type of plant it is?

It was found in Malaysia in my school compound

I have no idea how to start

You probably need an "identification key", or some kind of guide, that will help you identify the plant based on a series of questions or identification criteria.

To be able to use such keys or guides, you will need to familiarize yourself with technical vocabulary used in plant description. Some idea of the kind of ecosystem where the plant lives in would likely help too.

If the plant seems common, you will maybe find it on listings of common plants for your area.


how cells make other macro molecules? We know that the nucleus of the cell is the White House of the cell and its DNA is the president and it commands to make protein. So my question when DNA only codes for protein and enzymes,after the birth of a new cell where does the cell get lipids and carbohydrates to make membranes, organelles, water, ions, plasma membrane etc ...?

Molecules like complex lipids and carbohydrates are all synthesized by a special class of proteins that catalyze chemical reactions, called enzymes. Since the information of these proteins is coded for in the nucleus, you can imagine that ultimately the synthesis of these molecules does boil down to the genome.

The basic building blocks that the enzymes use to synthesize complicated molecules come from things you eat. Of course, we eat things that were once alive, and so the molecules that we get have been built up through enzymatic processes in the organisms we eat.

Ultimately, the "pre-organism" source of most of our molecules is CO2 from the air. Plants and photosynthetic algae have proteins that allow them to use the energy of the sun to reduce the carbon, making useful compounds such as glucose.


Does the DNA sequence of a butterfly match that of the caterpillar it used to be? Just had this thought occur to me.

If one were to take a DNA sample(or is it RNA?) of a caterpillar before it became a chrysalis, and attempt to match the sample against one taken after the chrysalis matured to a butterfly, would the two samples come up identical?

The genome (entire DNA sequence) of the butterfly would be identical to that of the caterpillar in all somatic cells.  A caterpillar has the genes to produce wings, for example, however at that stage in it's development they are not 'switched on' to make the necessary proteins.

If you were to sample the mRNA produced from transcription of the DNA in the caterpillar and butterfly stages, there are likely to be many differences.  As in the example I previously used, the mRNAs that are translated into wing-forming proteins are more likely to be apparent in the butterfly than the caterpillar.  When saying this, please be aware that I'm assuming that the regulation of these genes is pre-transcriptional - I'm not an expert of butterfly physiology!


How to get sulfate reducing bacteria? How can I find and get sulfate-reducing bacteria? Where and how can I store them for a long time?

Sulfate-reducing bacteria are everywhere, one spoon of soil contains several different species of them. The problem is how to isolate them from the other bacteria.
This old paper explains how to do it, I am sure there are newer techniques to do the same, it's up to you to dig into the literature to find the one you prefer if you want to isolate them by yourself.

Otherwise, just buy it from a collection.


Could Junk DNA be used as a Turing Machine by nature? In what ways has DNA been studied to see if there a "programmable" aspect to it?

Has nature produced anything resembling a Turing machine within the cell, perhaps using the "junk DNA" as its code? I expect nature's way would probably be very round-about and not compact.

NOTE: I am not asking about building DNA computers, as this question had recently been contorted to become.

Perhaps this question is whether the regions between genes sometimes known as 'junk DNA' has any function.

In the human genome, out of ~5 billion bases there are something like 20-30,000 genes which take up perhaps 10s of millions of base pairs, depending on how you count it. 1% of all human DNA is the common figure.

It is sometimes asked as if biologists commonly think of it as having no use, but in fact this is a researched topic, and few feel that it has no evolutionary or biological function at all.

Some of the most common uses for intergenic DNA in eukaryotes (bacteria are an entirely different topic with very different responses.

Transcriptional Regulation

Outside the coding sequences of the gene, there can be an extensive set of binding sities for proteins which regulate the gene.  In this paper in Figure 1 the celebrated regulatory sequence of ENDO16 is can be seen in Figure 1. As you can see for almoat 2000 bp there are numerous binding sites for many sorts of promotors and inhibitory factors, as well as factors which may splice the gene in various ways.

As I recall, ENDO16 only  turns on for a brief period in the development of the sea urchin and so its very tightly controlled, which means that its got a lot of regulatory elements upstream of it, controlling transcription. Its one of the most exhaustively studied genes ever and the believe they have most of it.  Other human genes ive seen perusing medical literature have seen 20kb are necessary to reproduce the regulation of a gene. Still all this might at best only triple the amount of DNA actively involved.

Centromeres and Telomeres
The physiology of the chromosomes have large regions as Deniz mentions are necessary for cell reproduction and for development.  In animals (like humans) the regions are devoid of transcribed genes and might be 10-15% of the genome length (I'm eyeballing this from the UCSC genome browser on chr21 - in some organisms like yeast the centromere can be just a few hundred base pairs.  So anyway we are getting somewhere now!
Non translated genes.
There are lots of pieces of DNA that might be copied into RNA and then do not function as templates for proteins.  some folks say there is a lot of this stuff.  The typical view is that there are a few thousand of these sorts of beasts known, and humans are currently thought to have about 1500 of them.  A small tweak in the number of genes, but they are there nonetheless.
Chromatin binding and organization sites
Although Centromeres are places where chromatin binds, the several families of proteins which bind DNA and wrap them into organized coiled coils thought to be like spools of telephone wire to form the Nucleosome which makes the chromosomes look like the little stick men you see in text books.  Chromatin can spool up just about any sort of DNA but seems to have a preference for regions which are at the ends of genes.  They can be modified by enzymes (acylated, methylated) to modulate their affinity for some classes of DNA sequence.  This is a hot topic of research.  The ability for RNA polymerase to find transcribe a gene is not good if its wound onto chromatin and though its not a precise binding like a transcription factor, chromatin binding and regulation must be affected greatly by changes in the distance between genes and the DNA sequences which surround a gene for thousands of base pairs, which is one of the main differences between species.

Of all biological systems (at least that I know of) this one accounts for the most bulk DNA sequence and is probably as related to the difference between different species as transcription factors and almost certainly is an older system of gene regulation, if you think about it.

Copy Number Variations and repetitive regions
just a side note, but small and very long repeat sequences can show up in the intergenic regions as well as inside a gene boundary to account for some of the differences between individuals.  they can be quite short or quite long.

Well hope this helps?


What is the main difference in chromatin fiber and chromonema? What I understand is both are coiled version of DNA along with histone but are termed different based on their degree of condensation. My question is when do we call it chromonema and when chromatin fiber? Do we consider 30nm fiber as chromatin and 10nm fiber as chromonema or something else?

10nm fibres are seen only by electron microscopy,while chromonema fibres refer to chromatin fibres visible by light microscopy. See this paper. 10nm or 30nm fibres are thus much, much smaller than chromenema fibres. There are likely several layers of organization (like 100nm and 200nm fibres) before you get all the way up to chromenema fibres.


Null distribution of Blomberg's K I've noticed different functions in different R libraries have different ways of assessing significance for Blomberg's K. For instance, picante's phylosignal looks at a distribution of PIC variance values from shuffled trait values to assess significance; when phytool's phylosig calculates a null distribution of Blomberg K values for shuffled traits.

What is the interpretative difference between the two and when should one approach be used over another? And what does it mean if the observed Blomberg's K is greater than 1 (traits less similar than expected under Brownian Motion model of evolution), but significantly greater (or less) than the null distribution of Blomberg's K-values?

The methods should be equivalent, given the same data. Using phylosignal's demo:

library("picante")
library("phytools")

set.seed(5)
randtree <- rcoal(20)
randtraits <- rTraitCont(randtree)

phylosignal(randtraits[randtree$tip.label],randtree)

phylosig(randtree, randtraits[randtree$tip.label], method="K",test=TRUE)

phylosignal returns:

         K PIC.variance.obs PIC.variance.rnd.mean PIC.variance.P PIC.variance.Z
1 1.430635          0.01147             0.4631411          0.001      -2.662701

and phylosig:

$K
[1] 1.430635

$P
[1] 0.001

Both give K = 1.430635 and an identical P-value.

Mathematically, it shouldn't matter if you shuffle the trait values or generate a null distribution of K. To get a null distribution for K, you have to shuffle something, and the tip values are probably being shuffled. You could check the code to be sure. An analogy is that, when doing a randomization for an ANOVA-like test, you can either shuffle the observed values or the group membership. Either way will give the same answer.

As for interpretation, Brownian motion is the simplest model for trait evolution, implying no direction, optima, rate changes, etc. K = 1 when the observed variation equals the expected variation. If K is greater than 1 then neighboring tips tend to resemble each other more than you would expect, suggesting a deviation from Brownian motion.


Where do migratory birds go when it rains? I was reading a comic from XKCD which inspired me to ask this question: "well, where do they go when it rains?" I know that when it rains you usually don't see any birds flying through the sky.

I imagine they normally hide in trees or under other kinds of cover. But for migratory birds, I don't think it is possible to hiding under cover until the rain passes. There might not be any cover (trekking across seas) or it might stay rainy for a very long time (and therefore cold...).

I did some research, but the answers are conflicting. Some people say they do stay in trees, others say they AVOID trees (because trees can snap in a storm, plus if there's lightning then sitting in a tree will net fried birds). Then there's people saying that birds have a waterproof coating... but that's a bit contradictory with me not seeing birds when it rains.

So where do birds go when it rains?

I assume that different bird species and groups of birds will behave in different ways. I am interested in the case of migratory birds because they are likely to encounter different climates and have perhaps devised strategies to be safe. I would appreciate any well-referenced examples.

Obviously, as you point out, some birds, such as waterbirds (ducks, puffins, auks, sandpipers) are perfectly fine in the rain, as they spend much of their time in the water anyhow and have oil glands that waterproof their feathers.

For other birds, rain can increase heat loss. For instance, rain increases metabolism by up to 22% in eagles (Stalmaster & Gessaman, 1984), although the actual impact on average daily metabolism was 'negligible'. However, eagles were able to feed their offspring only half as much, and therefore had only half as many eaglets, when it rained (Elliott et al., 2005). (On the other hand, the authors point out that in the Tropics, eagles actually do better when it rains because there is more food available).

Migrating birds stop migrating, hide where they can, and wait until it dries up before they continue (Erdi et al, 2002); those that don't, often end up far away from where they should be and, eventually, dead. In short, some birds don't mind the rain (e.g. seabirds), others sit it out in misery (e.g. nesting eagles) and others hunker down wherever they can find shelter (e.g. migrating birds).


On which DNA strand is TATA box present? My book (Snustard and Simmons) mentions that TATA box is present on the non-coding DNA strand but that was for the promoter of mouse thymidine kinase gene.

I have tried to find out more information and stumbled upon these in wikipedia articles which actually said something else:

  The TATA box can be an AT-rich sequence "located at a fixed distance upstream of the transcription start site. (from a paper "The RNA Polymerase II Core Promoter'')

Then (from a book: Understanding bioinformatics),

  The Transcription start site is the location where transcription starts at the 5'-end of a gene sequence.

So my question is, on which strand is TATA box actually (or generally) present?

TATA box is a feature of organisms that have dsDNA as a genetic material. Like most dsDNA promoter elements, TATA box is basically a section of dsDNA.

However a question like "On which DNA strand is TATA box present?" depends on what you define TATA-box as.

If you go by this definition:

  In molecular biology, the TATA box (also called the Goldberg-Hogness
  box)[2] is a DNA sequence (cis-regulatory element) found in the
  promoter region of genes in archaea and eukaryotes

then TATA-box is merely a DNA sequence and is just a representation of a ssDNA region. However, TATA-box is also the binding site for TBP (TATA-binding protein; part of the TFIID complex). While the recognition of DNA elements by the TFs is effectuated by the interaction of amino acid residues with DNA bases and backbone on  one or both the strands, the TF binding and its activity has a stereochemistry.

Likewise, TBP also interacts with bases as well as the sugar-phosphate backbone on both the strands (Juo et al., 1996; PDB:1TGH).

  Figure 2. Stereo pair drawings of the human TBP/DNA complex, with TBP at right and the sharply bent C-G-T-A-T-A-T-A-T-A-C-G duplex at left. (a) Molscript skeletal drawing (Kraulis, 1991). TBP residues that interact with the floor of the minor groove are shown in red with one-letter amino acid codes, and residues that interact with the sugar/phosphate backbone are shown in green. The coding strand of DNA is dark blue, and the non-coding strand is light blue. The two yellow-green base-pairs at bottom are the T1-A2 step that is kinked by interstitial phenylalanine residues, while the equivalent kinked step at T7-A8 is marked in orange. (b) Secondary structure diagram, with a-helices as coils and b-sheet strands as flat ribbon arrows pointing along N-to-C chain direction. Color coding as in (a).

Considering this, you can say that TATA-box is essentially a dsDNA region.

However, another twist in the story is that TBP can also activate genes with TATA-less promoters (Kamenova et al., 2014) and this is possibly facilitated by other protein partners of TBP in TFIID complex.

  Our results are consistent with the model that sequence-specific
  TBP-DNA contacts are not important at yeast TATA-less genes and
  suggest that other general transcription factors or coactivator
  subunits are responsible for recognition of TATA-less promoters. Our
  results also explain why yeast TBP derivatives defective for TATA
  binding appear defective in activated transcription.

This, still does not contradict with the fact that TATA-promoters need TBP and the binding is on both the strands.

So, my conclusion is that TATA-box is a dsDNA element but has a polarity in its mode of action.


The suspended cat clavicle I know the clavicle of the cat floats freely as opposed to be attached as in humans. This is supposed to allow them to be able to squeeze through spaces, according to a quick google search. But how does that allow them to move through tight spaces in comparison with humans?

Based on what I learned from my comp vert anatomy class, the clavicle does not articulate with other skeletal elements, thus allowing the scapulae to retract further along with the forelimbs


Can the Quarternary Extinction event be linked to the spread of mankind around the world? Evidence is presented in a variety of media by Paul S. Martin as his 'Overkill hypothesis', particularly in Twilight of the Mammoths.

The internet describes this idea as 'controversial.' Other than the works of Paul Martin, what evidence has been presented supporting this hypothesis?

Only in islands can this hypothesis be supported.  But islands are NOT continents, and that raises problems with the hypothesis.  The most inconspicuous of which is timing.

In Australia, the gap between man setting foot on Australia and the extinction of Australia's megafauna was 17,000 years. Too long.

Man left Africa and set foot in Eurasia more or less than 50,000 years ago, yet the extinction of Eurasia's megafauna happened 10,000 years ago. Too long.

The oldest discovered American, "Eve", was discovered in a cave in Mexico's Yucatan Peninsula and dated to be 13,500 years old, 500 years older than the supposed time that man crossed Beringia. This could imply that man crossed Beringia at a far earlier date, yet the dating of the extinction of America's megafauna coincided with that in Eurasia. Too long.

There's also into consideration the Younger Dryas climate chaos phenomenon, which did coincide with the extinction of the 30 genera of Pleistocene megafauna, a handful of microfauna and plants, not to mention the Clovis culture itself.

If man was the cause of the extinction event, the gap between man setting foot in new lands and the megafaunal extinction would've been a few generations, not a few millennia.


Does your iris color have an effect on your vision? I've always wondered if having different iris colors, (eye colors) may have any advantages or disadvantages on ones vision. Specifically regarding the effects of light.

Personally, I have troubles being out in the bright sun without sunglasses. My girlfriend on the other hand does not share this issue. Coincedentally my eyes are a light blue and hers are brown. After realizing this, I began to notice a trend when it comes to blue eyed people having this same issue.

So, on a bright day, does a person with blue eyes have a higher sensitivity to the light than their darker counterparts?  Thank you.

Firstly, note that "eye color" is actually iris color.

The person with a lighter iris will have more straylight compared to person with brown iris:

The graph represents Intraocular straylight of the age-matched groups. Participants with light-blue-colored iris showed significantly higher values for intraocular straylight than those of the other groups.

  Persons with light-blue-colored eyes have significant higher IOSL
  (intraocular straylight)
  values than persons with darker-colored irises (blue-grey,
  green-hazel, and brown). Light-blue-colored eyes had 0.07 to 0.08 log
  units higher IOSL values, which is an increase by a factor of 1.2. In
  regard to CS (contrast sensitivity), subjects with light-blue iris color showed also lower CS
  values than subjects with other iris color.

Edit: The study concluded that in people with blue irises, IOSL was significantly higher. Although IOSL did not affect best-corrected visual acuity (e.g. visual function based on a standard letter chart test at the optometrist), it did affect contrast acuity, meaning that folks with blue eyes had more difficulty assessing contrast differences (e.g., telling apart two grays with a slightly different brightness).

Christian Nischler & al. Iris color and visual functions. Graefes Arch Clin Exp Ophthalmol (2013) 251:195–202.


How do I interpret this depiction of dopamine neuron signaling? I am studying the work of Wolfram Schultz on reward signals. He depicts dopamine reward signals as shown below, which I do not know how to interpret. Each dot represents an action potential in a dopamine neuron, but is each row a different trial of the same neuron, or is each row the activation pattern of a different neuron? And are the bars at the top showing a sum of the count of the action potentials at each time step?

Schultz, W. (1999). The reward signal of midbrain dopamine neurons. Physiology, 14(6), 249-255.

From the figure caption for that figure:

  Each line of dots shows one trial, the original sequence in each panel being from top to bottom.

The bars at top are a summed histogram. Dots mark the time of spikes (this is called a "raster"). Each line is a different single trial from the same neuron.

(also note: this type of paper is called a 'review' paper, i.e., it isn't original research, although the original research might have been done by the same author. That doesn't mean anything bad, reviews are an excellent place to start understanding a topic, but you should be aware that the figures here are just representative examples or in some cases schematic diagrams. There is a lot of other data behind the conclusions drawn besides these single examples)


Why don't rats have a gallbladder, unlike other rodents? It has long been known that rats do not have a gallbladder, though other species including humans, monkeys, cows, reptiles, dogs and mice, all have a gallbladder.

In this paper from almost 100 years ago, scientists were studying what differences the presence or absence of a gallbladder gives the composition of bile. The authors found (what we now appreciate very well) that bile from mice who have a gallbladder was much more concentrated than rat bile - i.e. one of the functions of the gallbladder is to concentrate bile.

I know this is a very speculative question, but is it known whether having or lacking a gallbladder confers some sort of evolutionary or biologic advantage (or disadvantage)?

There are many different theories on this aspect of evolution, some of them are proved and others are just conjectures. Materials and research in this particular aspect is very few. Here I tried to provide an answer in reference to the particular animal you mentioned, i.e. rat.

Rats don't have a gallbladder possibly due to the following reasons -

The concentrating power of bile in rat's liver is high, so the main function of bile concentration by gallbladder is unnecessay in them. This is probably the most supported theory regarding this.
Rats frequently take their food so they require a continuous supply of bile. This eliminates the necessity of bile storage.
Harbivore animals relatively lack fat in their food. This reduces the need of large amount of bile salts in the intestine.

References -

https://theparadigmshiftgroup.com/animals-no-gallbladder/
Zoology textbooks
http://www.sciencedirect.com/science/article/pii/S0375090613000323?np=y


What is the most effective way to eliminate silverfish (g. Thysanura) from walls and floorboards? I've had our home fumigated, but the silverfish seem to return unaffected.

Are their eggs unaffected?

What's the best way to eliminate them from your home?

They feed on fungi, which grow wherever there's high humidity levels. So the best way to get rid of them would be to lower the air humidity. For example, by increasing the temperature in your (presumably) bathroom.


Why do eukaryotic organisms have introns in their DNA? We touched on introns and exons in my bio class, but unfortunately we didn't really talk about why Eukaryotes have introns. It would seem they would have to have some purpose since prokaryotes do not have them and they evolved first chronologically, but I could easily be wrong. Did the junk sections of DNA just evolve there by some sort of randomness or necessity as opposed to an actual evolutionary advantage? Why hasn't evolution stopped us from having introns since they seem to be a 'waste' of time and DNA? Why do prokaryotes not have introns?

There is still a lot to be learned about the roles introns play in biological processes, but there are a couple of things that have been pretty well established.

Introns enable alternative splicing, which enables a single gene to encode multiple proteins that perform different functions under different conditions. For example, a signal the cell receives could cause an exon that is normally included to be skipped, or an intron that is normally spliced out to be left in for translation (the Wikipedia article on the subject has a basic overview of the possibilities). This would not be possible, or at least would be much more difficult, without the presence of introns.
In recent years, we have discovered that RNA molecules (especially small RNAs such as siRNAs and miRNAs) are much more involved in regulating gene expression than previously thought. Often the small regulatory RNAs are derived from spliced introns.

There is probably more, but essentially introns enable a finer level of regulatory control. Biological complexity is often not the result of having a larger complement of genes, but of having additional layers of regulation to turn genes on and off at the right times. Prokaryotic genes are often organized into operons, and a single polycistronic mRNA will often encode multiple proteins from multiple adjacent genes. Since the biological processes required to sustain microbial life are much less complicated than those required to sustain eukaryotic life, they can get away with much less regulatory control.


Evolutionary distance between Canidae, Felidae, and Rodentia Comparing the families Canidae and Felidae, which have the shorter evolutionary distance to the order Rodentia? Less sophisticatedly put, are cats or dogs more related to rodents?

Online Ressources

Here is exactly the kind of question where tolweb.org is your best friend. tolweb.org is one of the most updated phylogenetic tree online. It also contains tons of reference, very useful to understand controversy over some nodes. onezoom.org is another online source that offer you to seek through the tree of life. Also, onezoom shows only the tetrapods (incl. mammals, birds, amphibians, lizards, snakes, turtles). However, onezoom has an awesome display and is a great tool for displaying diversity (they use the total length (in years) of all branches within a clade) within a clade and the threaten index (IUCN (red list) categories).

Dogs, Cats and Rodents

You will find the placental mammals here (tolweb). As you can see, the cats and dogs are both carnivora, while a rodent is a Rodentia (as you said). This means that cats and dogs have a more recent common ancestor than does either the cat or the dog with any rodent. Stated differently again, cats are not closer or further to rodents than dogs are. There is exactly the same distance between cats and rodents than between dogs and rodents.

One onezoom, the carnivorans is presented as a sister group to the ungulates. I have no idea what representation is the most correct but in any case, cats and dogs are carnivorans and share a common ancestor that is more recent than the common ancestor shared by carnivorans and rodents. So again, there is exactly the same distance between cats and rodents than between dogs and rodents.


Failed attempts at changing ecosystem in order to preserve it? Have there been any notable tries in the recent past (think 20th century or later) to purposefully change any ecosystem in order to save it or some particularly species in it, but which have instead produced the opposite effect? I am sure there must have been, but can't bring any to my mind at the moment.

Like, for example, if you have an island that has some large felines, which frequently attack sheep that are becoming scarce, so the felines are starving and becoming scarce, too. So you introduce feral goats, which were supposed to provide meat for felines, however, goats were (a) too nimble for felines to hunt well due to, eg. geography of the island (too many rocks that goats can prance about, but cats not so well), and (b) ate all the grass that sheep still had. So the net effect was that sheep died out, cats died out and there remained a few goats.

I am aware of a number of cases, where these things could have happened due to humans not aware or not caring about the problem (eg. introducing rabbits in Australia), but I am wondering specifically about misplaced efforts to save/stabilize an ecosystem.

Perhaps not quite what you had in mind, but it seems like the introduction of the mongoose into Hawaii is close. In the late 19th century sugar planters introduced mongooses into Hawaii in an attempt to control rat populations. It turns out that rats are mostly nocturnal, and mongooses are mostly diurnal, so the two species rarely interacted. The mongoose population boomed and had a huge negative impact on native bird and turtle populations, since the mongooses would eat the bird and turtle eggs.


How do molecules signal pre synaptic neurons to activate? How do molecules signal pre synaptic neurons to activate? and also is it more the structure or the elements in the molecule that allows it to activate the neuron also how do molecules bind to receptors and same as last time what is more important to do so the elements in the molecule or the actual structure? please answer I cannot find the answer anywhere else expert answers are appreciated!

-Gus

Activating a neuron generally means depolarizing the neuron, sometimes depolarizing enough to trigger an action potential. In general, molecules activate neurons by binding to their cognate receptors in the neuron cell membrane. Sometimes the receptor is, itself, an ion channel. Other times the receptor initiates a cascade of events in the neuron's cytosol that end up modifying the cytoplasmic portion of an ion channel and thus opening the channel. In both cases, the channel is usually specific for positively charged ions (cations) (e.g. Na+ or Ca2+) whose concentration is greater outside the neuron than in the neuron's cytosol. Activation results when these cation channels open and allow positively charged ions to flow into the neuron. This entry of positive charge reduces the neuron's cell membrane potential, making the potential less negative. If enough positive charge enters, the neuron may be depolarized enough to trigger an action potential on the neuron's axon. This is what is usually meant by activating a neuron. It depends on the three-dimensional structure of the molecule (often a neurotransmitter) and the structure of the receptor. The binding of a signaling molecule to its receptor is usually non-covalent, often mediated by hydrogen bonds.


cell uptake prediction I'm generating random molecules I would like to know if they are able to pass through the cell membrane. Are there any ways (preferably computational) to predict cellular uptake of an organic molecule which is about 55 atoms?

Absorption, distribution, metabolism, excretion, and toxicity ADMET can be somewhat computationally defined but is largely secretive due to the money involved in drug discovery. FAF-Drugs2 will do basic ADMET. The Schordinger Suit provides a more indepth ADMET for a fee.


Identification of this spider? I find these in forests in Oregon, western half, though they're probably on the eastern half as well. They live under pieces of wood and bark, and have a small web across the ground. Mine will eat crickets, but I think they eat carpenter ants, termites, and maybe pillbugs/sowbugs. It seems about an inch long, red on the thorax and legs, and dark grey and slightly hairy on the abdomen. The closest to this spider I've found is sowbug killers -- they're in my backyard, but they're smaller then this spider and also are a light tan on a hairless abdomen, with lighter colored legs. The fangs also seem different shapes but I'm not sure about that.

This is very likely a species in the Amaurobiidae superfamily, and I agree appears to be Callobius severus (the hackled-band weaver or the hackledmesh weaver).

 Source: Bugguide.net

 Source: Kyron Basu 2012
Moldenke et al. 1987 provide a key to spiders of the Pacific Northwest. Importantly, they note:

adult genitalia are necessary for identifying species and separating
Callobius from Amaurobius.

For example, here is a picture of Amaurobius ferox (Hackledmesh Weaver)

 © Danny Steaven 2008

I've seen numerous sites conflate this species with C severus and actually I've seen sources that identify them both as the "Hackledmesh Weaver".

So although the OP's specimen strongly resembles Callobius severus, a scope is necessary to truly identify to species. This Penn State page provides good information regarding these similar looking species in the superfamily.

Callobius and Amaurobius species have similar life histories and behaviors. They are most often found in damp locations under bark, leaf litter, and stones, as well as in woodpiles and other protected areas.

Stephen Ellis Lew (2011)  produced an atlas to the genitalic morphology of the Callobius genus, and he proposed a morphological diagnosis that is more consistent with principles of homology than those previously in use. [See the link for his dissertation on the subject].
Callobius severus
Description:

Cephalothorax and legs = reddish to dark brown [Source].
Abdomen = dark to light grey with fine hairs; often with large, bilaterally mirrored paler spots.

Ecology:

Nesting woodland species commonly seen in the Pacific Northwest

McIver et al. (1990) suggests that this species of spider is one of many that is characteristic of young forests.

Is it Dangerous?:

Not according to this Penn state website:

The one verified record of a bite by an immature Callobius species resulted in pain, itching, swelling, redness, and nausea.

Vetter & Antonelli provide evidence for how to differentiate this species from the "more dangerous" hobo spider.

in the side view, the palp of Callobius males has large, conspicuous, pointed projections (Fig. 7).


Why is defibrillation in asystole ("flat line") useless? In most popular medical dramas, when a patient has a cardiac arrest and "flatlines" the doctors many times use a defibrillator to "shock the heart back into rhythm'. I know that actually, the proper protocol is CPR and epinephrine (if possible), and that you should shock rhythms such as ventricular fibrillation. But why doesn't shocking the heart in asystole help?

If anyone could please explain, that'd be great.

In layman's terms: an Asystole is not affected by the electric shocks of a defibrillator. A defibrillator is used when the heart goes in fibrillations because it actually CAUSES an asystole. The idea is that you basically reset the heart to a blank state so you can start normal CPR procedure to help the heart go back to a normal rythm. That's why you see them applying CPR between shocks.

sources:

http://emedicine.medscape.com/article/757257-treatment

http://en.wikipedia.org/wiki/Defibrillation#In_popular_culture (citation needed)

http://calsprogram.org/manual/volume3/section12/CV/08-CV7AsystoleTreatment13.html


Molecular Cloning- Blunt end restriction endonucleases I work in a microbiology lab where we do a lot of cloning. I have always used restriction endonucleases to cleave the DNA to have sticky ends and not blunt ends. I currently am working on a project that suggests using a blunt end restriction enzyme, such as EvoRV, and then to perform a T-tailing of the plasmid, pl4440. My question is why do I not treat my pcr'd insert with a restriction digest just like I would the plasmid as the protocol suggests? How do I know the insert has ends that are able to ligate into the plasmid if I don't design the restriction sites into the primers?

To know if the ends are compatible see compatible cohesive ends (isoschizomers) from NEB website.

If you are unsure then do a blunt end ligation. For blunting a sticky end (From the comments):

Use Klenow or Pfu polymerase (or any proofreading/high fidelity polymerase).

You can use Taq if you intend to to a TA cloning.


Senescence, immortality and evolution? Many have heard about the fabled "immortal" jellyfish, Turritopsis dohrnii, which doesn't die from aging (senescence) and can revert the aging process indefinitely. It is rather remarkable that only one, or very few species show this type of behavior.

I wonder if at some earlier point in evolution, when life was predominantly simpler and sea based, there were more species with this feature, but this "immortality" caused overpopulation and/or didn't allow for proper action of natural selection, meaning that "immortal" species didn't evolve much and got wiped out almost entirely by whatever phenomenon.

In this scenario, aging and dying from old age would be an important evolutionary trait which would allow for populations to maintain reasonable sizes and would allow for natural selection to impart changes.

I was wondering how plausible all of this is, since I'm not an expert in the area and know little about the appropriate technical concepts behind these things.

You will find here a very good overview of the main hypotheses that explain senescence.

I am not sure I will answer your question but here are some reactions to your post..

What you say has to do with species selection. Selection selects between various objects/units that differ. These objects may be genes, individuals, populations, species, etc… In other words, there are various level of selection or different units on which selection acts. Wiki

Generally speaking, it is often assumed better to think in terms of selection acting on alleles (gene variants) or on individuals. Therefore, we tend to think that selection acting on genes or on individuals is more effective than selection acting on species. However, selection acts on species and we should not necessarily discard explanation using the concept of species selection.

What you say, if I am not mistaken, if we consider a set of species that are either mortal or immortal, we would predict that selection would benefit the mortal ones. Stating differently, mortal species have some advantage over immortal species that allow them to not get extinct or eventually to speciate more.

However, I don't quite understand the reasons why immortality would be deleterious to species. You say that it leads to overpopulation. So would you expect that a population is lead to overpopulation due to immortality and suddenly disappear because it is overcrowded. It doesn't sound like a well formulated argument to me. You could however argue that mortal species have a much greater individual turnover allowing them to adapt faster to environmental change than would immortal species.


How are mitochondrial ATT (Ile) start codons translated as Methionine? In some vertebrate species, some mtDNA start codon sequences are ATT but these are translated as Methionine rather than Isoleucine. What is the mechanism for this non-standard translation?

The main example below is in a bird, blue crane (NCBI Genbank excerpt below). The NCBI data give the standard note on completion of the stop codon but there is no note about modification of the start codon. We have confirmed this ATT start codon from PCR-Sanger sequencing an independent sample. There are similar cases in other vertebrates (Aves, Squamata, Amphibia) such as ND2 in Goggia geckos (example 2 below, also independently confirmed by Sanger sequencing. In this genus the start codon DNA varies from ATT to ATA or ATC: 50/59, 6/59, 3/59). I think I have seen this in other mtDNA genes. In many other birds and reptiles ND2 starts with ATG.

Are these modifed post-transcription to ATG? If so how?
Could they reflect a variant of the mtDNA code where AUU = Met? Or where any AUX codon is recognized as Met.

Example 1. ND2 from Blue Crane (NCBI Genbank refseq excerpt)

LOCUS       NC_020572              16696 bp    DNA     circular VRT 18-APR-2013
DEFINITION  Anthropoides paradiseus mitochondrion, complete genome.
ACCESSION   NC_020572
VERSION     NC_020572.1
DBLINK      Project: 193816
            BioProject: PRJNA193816
KEYWORDS    RefSeq.
SOURCE      mitochondrion Anthropoides paradiseus (blue crane)
  ORGANISM  Anthropoides paradiseus

 gene            3970..5008
                 /gene="ND2"
                 /db_xref="GeneID:15088361"
 CDS             3970..5008
                 /gene="ND2"
                 /note="TAA stop codon is completed by the addition of 3' A
                 residues to the mRNA"
                 /codon_start=1
                 /transl_except=(pos:5008,aa:TERM)
                 /transl_table=2
                 /product="NADH dehydrogenase subunit 2"
                 /protein_id="YP_007624320.1"
                 /db_xref="GeneID:15088361"
                 /translation="MNPHAKLIFLTSLVLGTTITISSNHWMSAWAGLEINTLAIIPLI
                 SKSHHPRAIEAAIKYFLVQATASALVLFSSMINAWSTGQWDITQLNQPMPCLLLTTAI
                 AMKLGLVPFHFWFPEVLQGSSLTTALLLSTVMKFPPITILFLTSHSLNPALLTSMAVA
                 SAALGGWMGLNQTQIRKILAFSSISHLGWMTIIIMYSPKLTLLTFYLYSLMTITVFLT
                 LNTTKALKLSTMMITWTKIPTLNATLMLTLLSLAGLPPLTGFLPKWLIIQELTKQEMT
                 TAATIITMLSLLGLFFYLRLAYYSTITLPPNSTNHMKQWHTDKSTNTLIAIFTSLSAL
                 LLPLSPMILTII"

 3901 agtagagtca gctaaaaaag ctatcgggcc cataccccga aaatgatggt ttaacccctt
 3961 cctctacta**a tt**aacccaca tgcaaaacta atcttcctca caagcctagt cctagggaca
 4021 accattacaa tctcaagcaa ccattgaata tcagcctgag caggcctaga aatcaatact
 4081 ctcgccatta tccccctcat ttcaaaatcc caccacccgc gagccatcga agccgcaatc
 4141 aaatatttcc tagtacaggc aaccgcttca gcactagtcc tcttctcaag tataatcaac
 4201 gcatgatcta caggacaatg agatattacc caattaaacc aaccaatacc atgcctttta

Example 2. ND2 in Goggia (Gekkota, squamata) NCBI nucleotide locus ref.

LOCUS       KF666817                1424 bp    DNA     linear   VRT 09-SEP-2014
DEFINITION  Goggia lineata voucher MCZ R184778 NADH dehydrogenase subunit 2

The key point in understanding non-AUG start sites in mRNAs is the nature and role of the initiator tRNA.

There is a special initiator met-tRNA which differs in structure from all the elongator tRNAs in such a way that it — and only it — is recognized by the IF-2 type initiation factors (and not by the EF-Tu/EF-1 elongation factors). In a complex with the initiation factor and GTP it can bind to the ribosome at the P-site. Normally the ribosome will also be interacting with an AUG codon at the P-site, but in some cases it is not, so that initiation may still occur.

  Thus, the initiating amino acid is always methionine, regardless of
  the codon, because methionine is the only amino acid with which the
  initiator tRNA can be charged.

In the case of bacterial mRNAs, it has long been known that about 10% start with other codons, predominantly GUG. This can be explained by their relative position to the ribosomal binding site on the mRNA — the Shine and Dalgarno sequence. I imagine this is what happens in mitochondria.

In the case of eukaryotic cytoplasmic mRNAs, an initiator met-tRNA complex normally scans from the 5ʹ-end, initiating at the first AUG or first the first AUG in an ‘appropriate context’. The precise definition of an appropriate context is unclear, and on can imagine that in some cases such a context pauses the ribosome at a non-AUG codon, at which initiation begins.

References

“The Biochemistry of the Nucleic Acids”, 11th edition, Chapter 12 (1992) RLP Adams et al. — this has all the older original references, but not the recent ones.

Wikipedia entry on Shine and Dalgarno sequence.

Eukaryotic scanning model: Hinnebush review (2011)

Initiation in prokaryotes and eukaryotes Londi review (2015)

Related SE Biology Answer on initiation and elongation met-tRNAs (by me)


Do fruit juices have a diuretic effect & what governs this? Was just contemplating this.

Juices tend to contain a lot of sugar.

Does the body absorb all the sugar in juices?
If the body does not, that sugar must be excreted by the kidneys alongside water thereby causing a diuresis, right?

NB I realise even if there is a diuretic effect that is outweighed by the large proportion of water in juices. But my question is whether there still is a small diuretic effect

In short: Drinking fruit juice by a healthy person with a normal kidney function do not likely have any significant diuretic effect.

Even if you drink, let's say, 2 liters of 10% fruit juice within 30 minutes, it would likely take about 2 hours for all the juice to be emptied from the stomach into the intestine and absorbed into the blood. Sugar delivered from the intestine will gradually increase blood glucose, but this will be balanced by the glucose taken from the blood by the cells, so, the blood glucose will not likely exceed 11 mmol/L, when glucose can start to move from the blood into the urine and cause diuresis.

I can back up this by the glucose tolerance test in which you drink 1 cup (237 mL) of a drink with ~35% glucose (>3 times as much as in a usual fruit juice). 2 hours after the test, the glucose levels in a healthy person (without diabetes mellitus) will be lower than 7.8 mmol/L, so below the diuretic level (11 mmol/L).


How to selectively filter BLAST results for an endogenous retroviral LTR to retrieve members of the same ERV family? I'm running a local BLAST search on a HERV-K(HML2) LTR sequence in the human genome. I get thousands of hits.

I want to retrieve the hits that correspond to other HERV-K(HML2) LTR sequences only.

What alignment length/identity filters should I use on the hits to select LTRs of the same family? Insertions and deletions could easily alter the alignment lengths meaning the cutoff length for the filter I want isn't clear. I can work out what alignment length cutoffs remove what percentage of the results to identify big drops at specific cutoffs, but it hasn't been very helpful.

I don't think there is a definite answer to this problem, but here are a few things that might help you, apart from a simple length filter for the hits:

Filter for regions: since LTRs are repeats you might get multiple BLAST results from the same repeat region/locus (especially if your input sequence is smaller than said region). You probably want to keep only one hit per region
Check for a conserved (sub)sequence: hopefully your specific LTR sequence has a 'core' that needs to be present, so that it can be considered part of your familiy. You only want to keep BLAST hits that have an absolute match for this 'core'.


What is the acceleration profile of a cheetah? I'm interested in the time it takes for a cheetah to reach maximum velocity as well as the acceleration over time that's typical of a cheetah prior to attaining this peak velocity.

According to a recent paper published on Nature, cheetahs can reach a top speed of 29ms-1 and very impressive accelerations, up to 100ms-2:

  The mean top speed was 14.9 +- 3.4ms-1 and was usually only sustained for 1–2 s. The highest speed we recorded was a stride-averaged 25.9-1

Also impressive are the lateral accelerations:

  Hunts involved considerable manoeuvring, with maximum lateral (centripetal) accelerations often exceeding 13ms-2

Here is the acceleration and speed chart:

The paper has several other charts: Locomotion dynamics of hunting in wildcheetahs


Understanding a Chromosomal formula in a karytope analysis I am reading a medical reporting results of a karyotype analysis. On it it is written:

Chromosomal formula
46,XX,del(7)(q11q36)[12]/46,XX[13]

I understand that 46 is the number of chromosomes, XX refers to the pair of sexual chromosomes, del(7)(q11q36) means a deletion on the long arm of chromosome 7 spanning the bands 11 to 36.
What do [12] and [13] mean?

Cytogenetic nomenclature is standardized in the International System for Human Cytogenetic Nomenclature. Unfortunately it is not free and my institution does not have access. However, looking at a preview of the 2013 version in Google Books, it would seem that the number in square brackets is the number of cells scored with that karyotype.


Is this ventricular tachycardia? I am investigating the public data of this.

Its specification

201 2 360 650000
201.dat 212 200 11 1024 972 -519 0 MLII
201.dat 212 200 11 1024 982 30947 0 V1
# 68 M 1960 2851 x1
# Digoxin, Hydrochlorthiazide, Inderal, KCl
# The PVCs are uniform and late-cycle.  Junctional escape beats occur following
# episodes of ventricular trigeminy.

The data is taken from the interval $[200000, 205000]$ in the following picture with the sample rate 500 Hz.

There seems to be more than Premature Ventricular Contractions (PVC), extrasystoles, so possible ventricular tachycardia.

The same patient has six minutes later this

I think you can see clearer here those PVCs, when the ventricle is starting to contract too early.

Both are very pathological situations.
How can you differentiate between the two?

Are there PVCs in both pictures?

I have looked at this ECG using LightWAVE.

The first part is showing atrial fibrillation or flutter with variable conduction because:

arrhytmia
no P waves or coarse fibrillatory waves
tachycardia at about 95-100 beats/minute
can be seen better in V1

Sample from 00:00:40

The second part is showing premature ventricular contractions with trigeminy because:

different morphology of QRS - ectopic
wide QRS
two normal complexes followed by one ectopic
presence of the compensatory pause after PVC

Sample from 00:09:20

References:

ECG data: PhysioNET MIT-BIH Arrhythmia Database
ECG criteria: LearnTheHeart.com