Do IgM and IgG differ for different infections? I am not that much educated in the medicine and immunology fields. So I noticed that there are tests for IgM and IgG immunoglobulins for various infections. I was not able to google quickly if IgM for one type of infection differs from the one for another type of infection.

I guess they differ because otherwise there would be only a few tests in the laboratory instead of dozens. But it would be great to hear some solid explanation.

IgM (Immunoglobulin M) is the first antibody to appear in response to an antigen. It can be produced by the fetus and cannot be crossed by the placenta.

Typically one might test IgM to diagnose hereditary and acquired IgM immunodeficiencies or diagnose Waldenstrom macroglobulinemia. It can serve as the earliest Ig serologic diagnosis of infectious disease.

Lab tests for IgM may be increased in liver disease, chronic infection, hyper IgM syndrome, and secondary to nephritic syndrome; Waldenstrom macroglobulinemia, lymphoma, CLL, multiple myeloma (rare), Schnitzler syndrome, cold IgM antibody agglutin, and MGUS.

Lab tests for IgM may be decreased in protein-losing syndromes, non-IgM myeloma, and infancy/early childhood.

IgG (Immunoglobulin G) activates complement and fights infection. IgG represents 70-80% of the total serum immunoglobulins in normal adults. It exists in four subclasses (IgG1, IgG2, IgG3, and IgG4). IgG1 predominates as 65% of the total IgG. IgG of maternal origin provides passive immunity to the neonate. It is transported across the placenta.

Typically one might test IgG to diagnose IgG myeloma, diagnose hereditary and acquired IgG immunodeficiencies, and provide a serologic diagnosis of infectious diseases and immunity.

Lab tests for IgG may be increased in multiple myeloma, solitary plasmacytoma, MGUS, lymphoma, CLL, sarcoidosis, cirrhosis, autoimmune diseases, parasitic diseases, chronic infection, and intrauterine contraceptive diseases.

Lab tests for IgG may be decreased in protein-losing syndromes, pregnancy, non-IgG myeloma, Waldenstrom macroglobulinemia, primary immunodeficiency states, and agammaglobulinemia (if combined with other immunoglobulin decreases).

Sources:
https://5minuteconsult.com/collectioncontent/2-152356/lab-tests/immunoglobulin-m-igm
https://5minuteconsult.com/collectioncontent/2-152354/lab-tests/immunoglobulin-g-igg


What is a cognate enhancer sequence? What is a cognate enhancer sequence?

While reading a paper (1) presented at a journal class in graduate school, I encountered this sentence:

  HIF-1 binds to its cognate enhancer sequence, the hypoxia-responsive
  element (HRE), and induces the expression of various genes related to the adaptation of cellular metabolism to hypoxia (the switch from oxidative to anoxic respiration),16 escaping from hypoxia (invasion and metastasis of cancer cells),17,18 improvements in hypoxia (angiogenesis)19,20 and the resistance
  of malignant tumors to chemo as well as radiation therapy.

(1) Is Wikipedia's definition of an enhancer correct for this case? Then does 'cognate' mean "related to, tending to be found together", whereas "sequence" means there's a chain reaction that occurs?

Y Zhu et al, "Involvement of decreased hypoxia-inducible factor 1 activity and resultant G1–S cell cycle transition in radioresistance of perinecrotic tumor cells" Oncogene (2013) 32, 2058–2068

Cognate means of common origin.

In molecular biology, cognate is used to refer to known interacting pairs of functional entities. For example, cognate receptor of a ligand means the primary (default) receptor with which this ligand interacts. Similarly, cognate sites (which also includes enhancer) of a transcription factor (TF) refers to the well known and validated binding sites of the TF.

Also see this post.


Blood group probability question My answer ( after rounding off) is 9% -100( 0.75 X 0.25 X 0.5) but the answer given is 22 %
Am I correct ?

I think the quoted answer is correct.

First, the probability of getting a son( and not a daughter) is $P_s=0.5$.
Next, since both the parents are heterozygous, the probability of genotype $hh$ is $P_h=0.25$. This genotype will not produce any antigen precursor, and hence there will be no antigens on RBC. As blood group O is defined by the absence of antigens, this can be classified as blood group O.For the expression of the antigen (dominant at the $H$ locus), the probability is $P_H=0.75$.

Again owing to the heterozygosity of both the parents at $I$ locus, the probability of getting a blood group with genotype $I^oI^o$ is $P_I=0.25$. This is the probability, that if the antigen precursor is made, $75%$% of the times the expressed blood group will be O. Therefore the probability of blood group O due to homozygous $I$ locus and dominant $H$ locus is $P_I\times P_H=3/16$.

Net probability for blood group O=(probability due to homozygous h+probability due to homozygous I and dominant H)*probability of a son.

$$P_{net}=P_s(P_h+P_HP_I)\approx 0.22$$


What is the mass of a pigeon tail feather? There is question at Space.SE If I drop a feather from orbit, would it burn up or “hit” the ground? there is an attempt to answer the question, but the mass of pigeon tail feather and possibly the drag coefficient is required to complete the answer.

I have looked around on the web and if there is an answer it is not jumping out at me.

What is the mass & drag coefficient of a pigeon tail feather?

I just weighed a pigeon tail feather (~10 cm) long. The mass was 0.05 g. Although all tail feathers are not equal in length (and all pigeons are not equal in size), this is probably a good approximation.

Measuring the drag coefficient is going to be very challenging, because it will vary with the orientation of the oncoming airflow. A feather falling with its broad surface (in this feather ~1.2 cm in chord width) perpendicular to the flow will have a much high drag coefficient than a feather falling with the broad surface parallel to flow.


In DNA sequencing, is "mate pairs" synonymous with "paired ends"? If not, how do they differ? By just looking at Roach et al's paper I get the impression that they are the same thing, and the Wikipedia URL for the former is a redirect to the latter.

However, I suspect they are not exactly the same - for starters, they wouldn't have two different words for the same thing, right?

Can anybody shed some light and suggest some references?

Thanks.

Paired-end is the name of the sequencing approach.

Mates refer to the read pairs that correspond to the same insert, but sequenced from opposite directions.


What do HG and NA mean in Geuvadis project RNAseq sample labels? I'm looking at RNASeq Data from Geuvadis website e.g. the file GD660.GeneQuantRPKM.txt.gz.

The samples are labeled by e.g. HG00105.1.M_120209_7 or NA20812.2.M_111216_6

What do HG and NA mean? Are they ethnic backgrounds?

If not, how can I look up the ethnic mapping to the samples?

Thanks!

If you google HG00105, among the first hits is geo accession GSM649517 with the title HG00105/NA12878.

Channel1:

Characteristics gender: Male
cell line: lymphoblast cell line HG00105
ethnicity: British from England and Scotland, UK (1000 Genomes codes: GBR)

Channel2:

gender: female
cell line: lymphoblast cell line NA12878
ethnicity: Northwest European American from Utah (HapMap code: CEU)

So no, they are not coding for the ethnic background but are part of the unique identifier of the sample.


Is this silverfish? My apartment very dry Can anyone please confirm whether insect below is a silverfish?  It looks a bit like the picture at our federal government pest control page.  It also moves with a wiggling motion, as described  at the Wikipedia Silverfish page.

I sprayed it with alcohol, and it seems to be dead.  I've seen this type of insect about once per month.  I don't know why they gravitate to my apartment, as the dehumidifier it set to maximum (35% relative humidity).

Sorry for the quality of the photo, but my iPhone SE does not have adjustable focus that I'm aware of. I can only tell the phone where the feature of interest lies within the picture.

Remi is right that it's a silverfish, and here's some macrophotography of Lepisma Saccharina.


What fills the space between the alveoli in the lungs? Do the lungs just consist of a large tree of alveoli, covered by the pleura, like this picture:

Or are they found "inside" the sac that is the lungs? If it's the later, what fills the space in-between the alveoli and forms the walls of the lung?

Alveolar tree is like a bunch of grapes. If you put a bunch of grapes into a plastic bag and put this bag into another bag, you can imagine how the lungs are covered.

Alveoli form the surface of the lungs. There is a membrane called visceral (or pulmonary) pleura that covers the alveoli and this membrane continues into another sheet called parietal (or thoracic) pleura that covers the inner side of the thoracic wall. The space between the membranes is called pleural space.

Here you can see how visceral pleura continues into parietal pleura:

Picture 1. Pleural space (source: sdstate.edu)

Picture 2. from page 1117 of "Cunningham's Text-book of anatomy" (1914) (source: Flickr)


Do hot drinks cool you down? It is quite the old wives tale that drinking a hot drink cools you down. If you don't really think about it it does seem somewhat logical: increasing temperature will cause your body to try and cool down faster. This is of course flawed by the fact that you have increased your temperature before cooling it back down again.

I have had a bit of a look, but have been unable to find any evidence that addresses the fact that drinking a hit drink may make you feel cooler after sweating a little bit, rather than actually changing anything about your net temperature. Basically, is the 'cool down' just the placebo effect (you feel cooler because you think you feel cooler), or is there any evidence for a 'real' effect of hot drinks cooling you down? Or is there evidence that hot drinks do nothing at all except heat you up a bit before you come right back to the same temperature?

A Study by Lee & Shirreffs addresses this question.  Unfortunately I only have the abstract, but it's enough to summarise from:

Method

Three groups exercised by  cycling before being given water at either 10°C, 37°C or 50°C.
They then continued to exercise until exhausted.
Mean skin temperature, core body temperature and heart rate were measured throughout.

Results

Mean skin temperature was highest in the hot drink category - half a degree warmer than in the cold group.
There was a heat difference between the two outlying groups of 33kJ.

Irritatingly the pre-drink temperatures are not included in the abstract so it's hard to compare the effect that the drinks have had.  Certainly the hot drink has warmed skin temperature above the thermoneutral group but I suppose that could be due to increased vasodilation leading to better core heat dissipation (as you suggest).

In absolute terms, you are warmer than you would have been after having a neutral or cold drink, however it could be that you feel cooler as your hotter skin loses heat energy at an increased rate due to the greater gradient.

References

 Lee JKW, Shirreffs SM. 2007. The influence of drink temperature on thermoregulatory responses during prolonged exercise in a moderate environment. Journal of Sports Sciences 25: 975–985.


What is the advantage of circular DNA in bacteria? From what I understand, bacteria have circular DNA. What advantages does it have over linear strands like for eukaryotes?

Do there exist bacteria with more than one ring of DNA?

Vibrio cholerae is known to have two circular chromosomes.

Bacteria cell division is a lot simpler and efficient as compared to eukaryotic cell division, partly due in part to the nature of their chromosomes. They don't have to undergo mitosis -- condensation of chromosomes, segregation, spindle fibre formation, attachment et al aren't involved in bacterial cell division.

Circular DNA also circumvents the Hayflick limit (thus allowing it to be "immortal"), which is the number of times a cell population can divide before it stops, presumably due to the shortening of telomeres, the sequences at the end of the chromosomes. Since circular DNA lacks telomeres, it does not get shorter with each replication cycle.

Circular DNA can also facilitate horizontal gene transfer such as Hfr mediated conjugation. Remember, conjugation is analogous to a "rolling-circle" type replication which is of course, only possible on circular pieces of DNA.


If dolphins can see sound, can they say images? Dolphins determine their surroundings by listening to echoes. Can they mimic those echoes and communicate it to other dolphins, transmitting an "image"? Does the same go for all echolocators?

As I understand your question, dolphins (and other echolators) can more or less map out their "surroundings" (which might include nearby ice floes, for example). It sounds like you're asking if they can then transmit that knowledge to other members of their species.

I don't know the answer, and I suspect no one does. However, it's hard to imagine why one dolphin would need to tell another dolphin about its surroundings when the second dolphin ought to be able to map its surroundings all by itself.

Cetaceans do communicate with each other, presumably alerting each other to danger (e.g. predators) and the presence of prey.

Incidentally, I worked on an acoustic study of bowhead whales in the Arctic Ocean years ago. We recorded bowheads and Arctic seals, which make some unbelievable sounds. We operated under the presumption that they were primarily "sounding out" their environment - searching for open areas in the ice where they could breathe, for example. It's possible that one whale might say "Hey, I found a breathing hole!" without mimicking the echoes that alerted it to that hole.

Sorry, that's not really a direct answer, but it might help put things in perspective.


What is this passage trying to say about Darwin's difficulty in explaining variation? This passage, from the book "How humans evolved" by Robert Boyd, says that one of the problems Darwin had at the time was that he struggled to convincingly explain how variation could be maintained; this was needed to theorize that evolution is the result of cumulative adaptations over many generations. According to the book, there are four problems, one of them being that selection removes variation:

  For example, suppose the environment changes so that individuals (finches) with
  small beaks are less likely to die than those with large beaks. The
  average beak size in the population will not decrease because there
  are no small-beaked individuals. Natural selection destroys the variation needed to create adaptations.

I understand the idea, but don't really understand what the example is trying to illustrate. The example seems to be saying if small beak finches survive better, then there would be no small-beaked finches...?

The second difficulty Darwin had was in explaining how animals "might evolve beyond it's range of variation (?)"

  Selection can cull away some characters from a population, but how can
  it lead to new types not present in the original population?

The bit above I understood; however, I struggle to see the point of the example that was given for it:

  How could elephants, moles, bats and whales all descend from an
  ancient shewlike insectivore unless there were a mechanism for
  creating new variants not present at the beginning?

Please help rephrase or explain again what these two difficulties actually are, or help make sense of the two examples that the book gave.

Remember this is all before the rediscovery of Mendel and the understanding of things like recessive traits and inheritance of discrete rather than blended traits. The problem is that, given an environment in which large beaks are beneficial, over geological time selection will tend to eliminate the small beaks. Then, if the geological environment changes such that small beaks are favored, there are no small-beaked individuals to benefit from the change: they would have been eliminated gradually during the long time when long beaks were preferred. The paradox or difficulty Darwin had was explaining how populations could maintain sufficient variability for selection to act to generate new traits.
This issue is similar to the first: the process of natural selection is all about what happens to existing populations. It explains what happens when you have variation existing in a trait. Natural selection by itself does not explain how mutations could occur to produce those new traits.

Darwin was concerned about both of these issues because at the time he saw them as serious threats to his theory (and specifically, like most good scientists, he worried that these things could mean that he was wrong). It seemed like a weakness of exactly the type he saw in prior works on transmutation of species that he was trying to work beyond. It took a few decades and a lot of scientific progress including the rediscovery of Mendel and the Modern synthesis for these problems to be truly worked out. As for Darwin, the best he could come up with was his somewhat-Lamarckian pangenesis idea, which he defended strongly.


How should "the human genome" be interpreted? What does sequencing "the human genome" mean? Don't individuals have unique genomes?

Certainly individuals have unique genomes. The human genome sequencing project used DNA from a handful of volunteers, and the reference human genome that resulted from this project can be thought of as an "average" genome for those individuals. Where sequences differed between the individuals, a representative consensus sequence was chosen. Hence, the sequence of a gene from a given individual may not perfectly match the reference genome, although mostly the differences are small: genetic difference between humans is estimated to be around 0.1 --- 0.4%, which means a few million base pairs in total.

As DNA sequencing is nowadays orders of magnitude cheaper, genomes for larger number of individuals are being sequenced; see for example the 1000 genomes project.


Why doesn't patients with chronic acne's body lower sebum production itself? Background
My cousin has had nodular acne for at least 9 years. Her sebum plugs usually causes bumps on, and inflame, the skin, before the sebum emerges or can be extracted with a comedo extractor. Occasioanlly, this happens without inflammation.
Dermatologist's Feedback
He said that topical retinoids open pores to help expel the trapped sebum, but only oral treinoin (E.g. accutane) can dwindle sebum production.
Question
We forgot to ask him why the body (on its own) doesn't slack sebum production ? We're assuming the body's ability to detect the inflammation and acne nodes, and to adjust sebum production?

Short answer there is no feedback mechanism to tell the body it is overproducing, inflammation can have a huge number of causes, many of which could actually be worsened by decreased sebum production.

Also "overproduction" is a misleading term; it is overproduction compared to the norm for the population and may be perfectly normal for that individual. It is like asking why redheads don't start growing black hair when surrounded by surrounded by people with black hair.


Can brain cells move? I was discussing this with my brother. I'm pretty sure I read somewhere that they can move.

Thanks

EDIT: By movement I mean long distance migration (preferably within the brain only).

The question is relatively broad and one should take into account that the brain not only consists of neurons, but also glial cells (supportive cells) and pre-mitotic neuronal stem cells. Furthermore, as critical fellow-scientists have indicated, developmental stage is very important, as the developing embryonic brain is very different from the adult brain.

However, after sifting through various publications, the answer to the question is actually remarkably simple: Yes, brain cells migrate.

In  the adult brain glial cells migrate in the brain (Klämbt, 2009). Glial cells are involved in a myriad of functions, but a notable example of migrating glial cells are the oligodendrocytes that migrate relative long distances to find their target axons onto which they wrap themselves to form the insulating myelin sheath (Tsai and Miller, 2002).

Neuronal stem cells migrate over long distances in response to injury (Imitola et al., 2004) and they migrate from specific stem-cell locations (e.g., hippocampus and subventricular zone) to other regions (Clarke, 2003).

Interestingly, post-mitotic (fully differentiated, not-dividing) neurons can also be migratory in the adult brain. Specifically, newly formed neurons can migrate over hundreds of microns in fish (Scott et al., 2012) and neuronal migration has been shown in the human cortex as well (Fox et al., 1998).

Not surprisingly, glial cells, stem cells and neurons also migrate during embryonic development. Most notably, post-mitotic neurons destined to fulfill peripheral functions have to migrate over relatively long distances from the neural crest to their target locations (Neuroscience, 2nd ed, Neuronal Migration).


Bilirubin metabolism and UGT1A1 inhibition in human vs. monkey? In human UGT1A1 seems to be the only relevant enzyme to glucuronidate unconjugated bilirubin into excreted forms. Is the pathway the same for e.g. the Cynomolgus monkey (Macaca fascicularis) in vivo? In case UGT1A1 is potently inhibited are there any other potential enzyme to metabolise/glucuronidate unconjugated bilirubin in monkey? Furthermore, bilirubin is analytically challenging in UGT1A1 inhibition studies in vitro. Estradiol (3-glucuronidation) has been used as a specific substrate for human UGT1A1. Do you know any substrates known to be specific for monkey UGT1A1?  Any reference would be highly appreciated.

UGT1A1 is common among most mammals that produce bilirubin (rats too). I haven't seen any evidence to suggest an alternate pathway in mammals of bilirubin metabolism. Look into gilbert's syndrome patients (they have a SNP which is a mutuation that causes UGT1A1 to be less efficient and thus a rise in plasma unconjugated bilirubin).

Also, bilirubin analysis from plasma/tissues is fairly straight forward with HPLC or LCMS assays. UGT1A1 inhibition in vitro however, is still a challenge. I think the trick will be to use CRISPR to knock it out.


What do the the different arrowheads mean in a cell signalling diagram? What do the different arrowheads mean in the figure below? Are there arrows upstream or downstream signalling?

Arrowhead interpretation
As I said in my comment and to add to @AlwaysConfused's answer, the arrowhead is a promotion, and flathead is an inhibition.
Typically, any other notation such as dotted lines would be explained in the figure legend of the illustration.
The below definitions are generally accepted and widely used.
But don't take these definitions for granted; there are no strict usage policies for these diagrams.
Different groups may use different nomenclature and symbols.

These definitions were taken from a legend in cellsignal.com.
Upstream and downstream
The arrowheads are not necessarily linked to up and downstream signalling.
Generally, the direction of the arrow indicates upstream/downstream.
However, at a glance, this has even less standardisation than the arrowheads.
Sometimes, like in the example in the question, upstream is generally at the top, and downstream is at the bottom.
Other times it is from left to right, or right to left.
There are many examples of cyclical events which the only way to tell is by following each arrow "path" for a particular signal.


Is there vascular supply to cartilage According to Gray's anatomy, cartilage is avascular but in a recent class, my teacher told me that there is vascular supply but it is confined to upper surface only. So, I'm confused that who is correct.

This depends on what kind of cartilage you are examining and where it is located. Cartilage is not all the same depending on where it is located and it's intended purpose. Cartilage also generally exists as a continuum with the bone that it is attached to where you will see transitional changes from bone tissue to cartilage without specific delineation. Depending on the cartilage location and its function it may of may not be vascular. Hyaline cartilage existing closest to synovial joint spaces is pretty much entirely avascular. This has some advantages and disadvantages. Damage to cartilage is very difficult for you body to repair for myriad reasons one being avascularity, but also the avascularity allows for you to transplant live cartilage to any person regardless of what tissue type the donor or recipient is.


Where is the line between Anaerobic and Aerobic? I am well aware of traditional anaerobic respiration (lactic acid or alcohol produced - no Krebs cycle) and traditional aerobic respiration (O2 is used at the end of the Citric acid cycle).

I am wondering how to classify respiration that uses the Citric acid cycle, but consumes a nitrite/ate or sulfite/ate instead of O2. Is that anaerobic or aerobic?

I could only find this image on Google image search catch but it said it was from http://lecturer.ukdw.ac.id/dhira/Metabolism/RespAnaer.html

Anaerobic respiration is a respiration where the final electron acceptor is different than oxygen. The final acceptor can be a less oxidizing than oxygen, like sulfate (SO42-), nitrate (NO3-), or sulfur (S). For example bacteria that use sulfate are obligate anaerobs.

The Krebs cycle cannot take place in the absence of oxygen, although oxygen is not directly involved in the cycle. The oxygen is required for the electron transport chain, which oxidized NADH and FADH2 back to NAD+ and FAD+, which are involved in the four reduction reactions of the cycle.

Thus, aerobic respiration includes both Krebs cycle and final electron acceptor of oxygen, whereas anaerobic respiration does not.


Online toolkit that provides functional similarity scores (in the form of a matrix) between two functional gene sets in the context of gene ontology Where can I find an online toolkit that provides functional similarity scores (in the form of a matrix) between two functional gene sets in the context of gene ontology?

I have tried the following:

Batch tool for GSFS: PROBLEM: It says that my input yeast genes are not human genes (which probably means that the tool will work only with Human genes).
http://bioinformatics.clemson.edu/G-SESAME/Program/geneCompareTwo1.php : PROBLEM: provides score for every gene pair input. I have ~3600 genes. Impossible to do it for eveyr pair.
DAVID batch viewer gives a 1xN matrix (functional similarity score of one gene to a set of N genes, when I want all possible pairs of similarities which will give an NxN matrix)
GO funsimmat- I am unable to get this to work, so I'm not sure if it will give me the desied results.
GO FastSemSim- same as 4.

I think that you could try a similar approach to GSFS:

use transduction in proteins (if you don't know star code, then you must use 3 strings for each gene)
use a basic tool (a stand alone like UNIPROT tools) to identify the proteic domain type (chain alpha, ..)
divide the genes by proteic domain type (pdt): which contains which pdt and the pdt order frequencies

Now, you could use DAVID or similar (try wconsensus: it's old, basic but very custom) to compare similar sequence and obtain your scores.


Does GABA help or hinder anxiety? This article

https://www.prnewswire.com/news-releases/smartphone-addiction-creates-imbalance-in-brain-300558945.html

Says both

  The researchers performed MRS exams on the addicted youth prior to and following behavioral therapy and a single MRS study on the control patients to measure levels of gamma aminobutyric acid, or GABA, a neurotransmitter in the brain that inhibits or slows down brain signals

And

  Having too much GABA can result in a number of side effects, including drowsiness and anxiety.

If GABA slows down brain signals, wouldn't that reduce anxiety? And if you have too much GABA, wouldn't that reduce anxiety also, not increase it?

DreamWater, a 5 Hour Energy counterpart, has GABA, 5-HTP, and melatonin, which promote sleep. It wouldn't make sense that GABA increases anxiety to promote sleep.

I wouldn't bother trying to interpret press-release science that doesn't even contain a citation or link to the original research. However, I will try to address some of the other content of your question.

It is indeed true that many anti-anxiety medications, particularly the benzodiazepines, act primarily to increase GABAergic activity by potentiating GABA receptors.

However, it is also true that GABAergic activity is not some monolithic attribute of the brain. Different brain regions have different functions, and some brain regions are associated with behavioral or neurochemical inhibition of other regions. An increase in GABA activity in a brain region that tends to inhibit others could theoretically be anxiety-inducing rather than anxiety-calming, even if the overall effect of increasing GABAergic effects is anxiety-calming. Looking at GABA levels is also only one part of the picture, and it fails to tell you a) how often GABAergic cells are releasing neurotransmitter, and b) how sensitive post-synaptic cells are to GABA. The overall effect of GABA is going to be roughly proportional to (GABA concentration) * (how often GABA is released) * (sensitivity to GABA).

An extreme example of why this is important are the delirium tremens that occur if a severe alcoholic suddenly stops drinking alcohol. Alcohol also potentiates GABA receptors, and with long term use the brain compensates by reducing GABA production. However, this adaptation is fairly slow, and alcoholics who quickly stop drinking can have motor symptoms and seizures as a result (some other neurotransmitter systems are involved as well, though, so this is a bit of a simplification). The opposite could be true as well: it's possible that increased GABA concentrations could be because not enough GABA is being released or because postsynaptic receptors have been downregulated. It is quite possible that you could have more GABA but less GABAergic inhibition. This study didn't test levels of inhibition, just levels of GABA.

Lastly, eating GABA to make you sleep is a bit silly and is far removed from brain levels of GABA or inhibition in the brain - I am not aware of any study that shows that eating GABA makes you sleepy; companies can freely put it in a drink and make abstract claims that suggest it aids sleep, but that doesn't mean it actually does, a beverage like that isn't regulated the same way that pharmaceutical drugs are.

In summary: be very wary of attributing a complex behavioral outcome to one particular element in the brain.


Kin selection Vs altruism (social biology) I know that this is a contentious topic and I found conflicting explanations online which is what prompted me to put his question up. In some papers, Kin selection is mentioned based off the concept of inclusive fitness (sum of direct and indirect fitness). However, Kin selection is said to be an altruistic characteristic. That being said, altruistic genes only propagate through indirect selection (since an actor gives up its own fitness and do not generally reproduce). In that case, isn't Kin selection based off just indirect fitness and not inclusive fitness as a whole?

In a webpage, it is mentioned that "Kin selection is the evolutionary mechanism that selects for those behaviors that increase the inclusive fitness of the donor.". In that case, how can kin selection be altruistic? Can someone shed some light on what Kin selection is exactly? Also, a proper definition for indirect selection would be good as well. Thank you.

how can kin selection be altruistic?

Part of you confusion is purely semantic.

Kin selection cannot be altruistic. Kin selection is an evolutionary process. Altruism is a behaviour. Saying "kin selection is altruistic" is like saying "natural selection is flying" (when thinking of selection for flying abilities in, say, flying squirrels).

Altruism

Altruism is a behaviour in which increases another individual fitness at the expense of its own fitness. However, this definition lead to confusion of whether one is talking to lifetime fitness or only to a contribution to one's fitness that will eventually be returned. For this reason people talk about True Altruism and False Altruism

True Altruism

True altruism is a behaviour in which the actors's (the one performing the altruistic behaviour) life time fitness is decreased while the recipient (the one benefitting from the altruistic behaviour) is increased.

True Altruism can only evolve via kin selection (or group selection for the few who still view these two processes as different).

It is the indirect component of the inclusive fitness that selects for altruism indeed.

False Altruism

False altruism refers to cases where the actor performs the behaviour because he is expecting (not necessarily consciously) a return later in life. False altruism can be seen as an investment.

Such false altruism can be selected by natural selection (no need to consider indirect fitness). "Return on investment" can be caused by direct reciprocity or indirect reciprocity. In case of indirect reciprocity, some populations can use a system of reputation, where individuals are more likely to help individuals that they have seen being helpful to others before.

Game theory

All types of interaction between individuals can be modelled in game theory. One can also investigate specific type of strategy in response to a a specific game. For example, Tit-for-Tat is one type of strategy in a multiple encounter between two individuals game.


What is this flat dry stick-like leaf that rattles? I googled those terms but came up empty, here are three photos with a ruler for scale:

The hole and scratches are my dog's teeth, so as you can tell, it is strong yet not brittle. When you shake it, it rattles, like maybe there are seeds in there.

It's from a public irrigated park in a Northern Hemisphere hot desert climate (BWh) region, and I picked it up today, so spring time if that will help.

My dog is usually the one to find it, and we play fetch with it.

I believe this a seed-pod from an Inga or Delonix plant.

Inga are native to South America, while Delonix are native to Madagascar. But they've been introduced to other places and I've seen similar plants in the northern hemisphere. Inda and Delonix are both members of the subfamily Caesalpinioideae. I found the name by searching for "seed pod shaker". Sometimes you just need to know what terms to google.

Shown in the image below is pacay, or Inga feuillei.

But your pod could also be from the flame tree, Delonix regia.


How do memory cells(B-cells) encounter pathogens? From what I understand, once the infection is handled, some of the B cells capable of producing the correct antigens are stored for the long-term in the lymph nodes.

They will start multiplying again upon encountering the pathogen again.

What I don't understand is how can these cells, that should be in relatively small numbers, can effectively encounter the pathogen ? Do all pathogens travel to the lymph nodes? Do the memory B cells travel out and encounter pathogens?

Great Question.

Location:
Memory B cells are highly abundant in the human spleen, and they make up 45% of the total B cell population in this organ. There is evidence to indicate that human memory B cells might mostly reside in the spleen, and some memory B cells recirculate in the blood [1].

Activation:

Memory B cells circulate throughout the body in a quiescent state until specific antigen is re-encountered and triggers a potent secondary immune response [2].T cell help is a strict requirement for the reactivation of memory B cells that are specific for monomeric protein antigens [3].

Sources:

Hauser, Anja E., and Uta E. Höpken. "B cell localization and migration in health and disease." Molecular Biology of B Cells (Second Edition). 2015. 187-214.
Firestein, Gary S., et al. Kelley's Textbook of Rheumatology E-Book. Elsevier Health Sciences, 2012.
Janeway, Charles A., et al. "Immunobiology: the immune system in health and disease." (2005).


Do any birds beside the family Columbidae (or any reptile or mammal) feed their young "Crop Milk" Birds from the family Columbidae (e.g., doves and pigeons) produce a fatty, milk-like substance in their crop.  The secretion is often referred to as "crop milk."  They feed crop milk to their young through regurgitation.  Does anyone know of another bird or reptile group (or even mammals) that has evolved such a mechanism; not regurgitation but secretion of a milk-like substance for feeding young?  Also, both male and female doves produce crop milk; are there cases where males of a mammal species produce milk?

In mammals there are only two species (known, there may well be others) where males lactate. They are both species of bats and this paper discusses the evolutionary mechanisms that could underlie male lactation. I have ignored human cases because they are more of an unusual occurrence (often brought on by severe dietary stress) rather than an evolved mechanism.

Other non-mammals include Flamingo and Penguins. There is also a species of fish, called a discus fish, which produces a mucus from its skin which the offspring feed on (here). I would hypothesise that this evolved originally for different reasons (defence, scent communication, excretion...) but offspring "discovered" this was slightly nutritious so fed off it, those genetically predisposed to doing such things then had higher fitness and the trait spreads. Evolution of greater or more nutritious mucus production would be achieved because parents that produce more/better mucus would have more offspring that reach maturity.

The paper by Kunz & Hosken is a good discussion on current evidence and the potential for evolution of male lactation.

I hope that answers your question, happy reading!


Can light function as a neurotransmitter? Any animal with an eye has photoreceptors, which are essentially light-sensitive neurons. Green algae have channelrhodopsin, which are ion channels that open and close in response to light. Clearly, the nervous system and its molecular components have evolved to use light effectively.

I'm wondering if light can act as a neurotransmitter in the classical sense; that is, the presynaptic cell releases a photon, which travels across the synaptic cleft and interacts with a receptor, depolarizing the postsynaptic cell. Light can be generated in vivo through chemiluminescence, and as with channelrhodopsin, different proteins can activate in response to different wavelengths or intensities. I suspect this would be much faster than traditional chemical signaling.

I don't think there is a theoretical reason why this wouldn't be possible.  However, I think there might be some practical problems with a system that relied upon light signaling.

1) It would be susceptible to interference.  Many bio-luminescent organisms are transparent, so other sources of light could depolarize a post-synaptic cell.  Light also penetrates tissue in organisms that are not transparent.  Blue light can penetrate 2 mm of human tissue and higher wavelengths like red can more than double that.  I could see light acting to replace signal molecules in quorum sensing though.

2) Neurotransmitters aren't really much of a limiting factor in nervous system speed. A monosynaptic reflex travelling a short distance might take 30 milliseconds, but neurotransmitter transmission is only 1 of those milliseconds.  In more complicated neural pathways, the speed of neurotransmitters might only account for 1/100th of the time.  So, if we're just imagining time-saving nervous system improvement, fiber optic neurons are the way to go.


Thermodynamics of Forming Peptide Bonds Which of the following shows the correct changes in thermodynamic properties for a chemical reaction in which amino acids are linked to form a protein?
A) +ΔH, +ΔS, +ΔG
B) +ΔH, -ΔS, -ΔG
C) +ΔH, -ΔS, +ΔG
D) -ΔH, -ΔS, +ΔG
E) -ΔH, +ΔS, +ΔG
Answer:  C

I know that dehydration is endergonic (+ΔG).
I have two questions:

Why is entropy decreasing? In the beginning of the reaction, we have two amino acids. By dehydration, we have at the end two molecules: the two amino acids together and the H2O molecule. The same number of particles before and after.

Why is enthalpy change positive? You made a bond between the two amino acids. That is exothermic.

The energy used to catalyze the peptidyl transferase reaction is from the breakage of the bond between the amino acid in question, and the aminoacyl-tRNA it's attached to. The two reactions are coupled by the ribosome. The ribosome can then lower the entropy by positioning of the molecules (including water) in the active site as described here.

So we have our reaction ΔG = ΔH - TΔS

Your ΔG is positive because your reaction is endergonic, and the ΔH is positive because the peptide bond is the system, and you're absorbing energy to form it. The entropy is decreasing as such (removing enerygy = removing heat from outside the system), and the actual reaction for the formation of a peptide bond is unfavorable. As I mention above, this unfavorable reaction is coupled to a favorable reaction in the hydrolysis of an aminoacyl-tRNA to make it possible. What I forgot to mention above is that the ribosome is making this more favorable as well by decreasing the activation entropy for the reaction, and that's what they describe in the linked journal.


Help id-ing creature I know. This is going to be extremely difficult without a picture. But bear with me here, because I haven't seen it afterwards. I hope somebody can give me a list of possibles.

I was taking a stroll down the street when I saw this creature. Maybe two feet long. It was black, with a tail about the size of the tail of a cat. It had catlike paws, which were not that big. Its face was pointy, with a reddish nose and brown eyes, with a whitish area of fur above the eyes. Ears were small and curved at the end. It was hiding in a bush, and did not seem to run away when I checked it out. When I got up, it made a sharp screech and ran away.

I'm from Kerala, South India. Thanks in advance.

sounds like a mongoose or a civet, which species is hard to guess there are several species of both in India, and they come in a variety of colors and sizes. In the mongooses the color can vary a lot even in the same species. One easy way to tell the difference is civets have cat like ears while mongoose have short rounded ears.

But here is a picture one at least one species of each, since their body plant does not vary much even if their color and size does.

Indian Brown Mongoose,

Sri-Lanka Mongoose

Asian Palm Civet


What benefits do sloths and manatees gain from algae growth on their fur/skin? Slow moving sloths and manatees have green algae growing on their fur/skin.  Are there any other animals that have algae growth on them, and does the algae benefit the fitness of these animals?

Source: Canadian Museum of Nature

Source: wildlife.org

I don't know about manatees, but sloths have a symbiotic relationship with the moths living in their fur because the moths supplement the sloth's diet with additional nutrients via algae. Sloth moths grow and die in a sloth's fur, decomposing to provide nutrients for the algae. The sloth then eats the algae. What the moth gets out of this is that its larvae can feed on the sloth's poop, and when they grow up, they make a home in the sloth's fur again.

Here's an infograph summarizing the relationship: http://www.pbs.org/wnet/nature/sloth-named-velcro-sloth-moths-mutually-beneficial-relationship/11159/


How to get Population Genotype Frequency from 1000 genomes Perl API Posted a similar question on Biostars but got no response. Not sure if I'm allowed to link to it? Basically I want to pull genotype frequency data for a population group (such as CEU) instead of allele frequency data, via the Perl API for 1000 genomes. I have tabix and perl API installed. This is for 100,000+ SNPs so the solution should hopefully not involve manually downloading genotype and calculating the frequency manually in a for-loop. My understanding also is no solution exists in BioMart (according to the Biostars answer).

Following the instructions here, I can see how to get specific genotypes for all individuals as a list.

Eg: Input -> Some snp, CEU... Output -> G/G 0.87, G/A 0.13 (frequency of some snp for CEU population).

I need to do this for 100,000+ SNPs, so I imagine manually pulling all genotypes for each SNP and calculating the frequency manually in a loop would not be practical.

If you want population specific allele frequencies you have three options: * For a single variant you can look at the population genetics page for a variant in our browser. This gives you piecharts and a table for a single site. * For a genomic region you can use our allele frequency calculator tool which gives a set of allele frequencies for selected populations * If you would like sub population allele frequences for a whole file, you are best to use the vcftools command line tool.

This is done using a combination of two vcftools commands called vcf-subset and fill-an-ac

An example command set using files from our phase 1 release would look like

grep CEU integrated_call_samples.20101123.ALL.panel | cut -f1 > CEU.samples.list

vcf-subset -c CEU.samples.list ALL.chr13.integrated_phase1_v3.20101123.snps_indels_svs.genotypes.vcf.gz | fill-an-ac |
    bgzip -c > CEU.chr13.phase1.vcf.gz

Once you have this file you can calculate your frequency by dividing AN (allele number) by AC (allele count)

Please note that some early VCF files from the main project used LD information and other variables to help estimate the allele frequency. This means in these files the AF does not always equal AC/AN. In the phase 1 and phase 3 releases, AC/AN should always match the allele frequency quoted.


How can you test what color different people perceive? If I would show someone a yellow object and ask them, "is this object yellow?"
 That person would say "yes".

But I could never know if my perception of the color yellow is the same as that other person's.
Because he or she could actually be seeing, what I know to be the color green.
But then tells me that its the color yellow because that has been taught to him or her from young age.

So how can you test if people are really seeing the same color?
(originally posted this question on physics.stackexchange but was advised to try it here)
https://physics.stackexchange.com/questions/48731/how-can-you-test-what-color-different-people-perceive

One way we can get evidence qualia are the same or very similar for different people is by reactions to it, beyond just the word.

For example, beyond the word "pain", we have other strong reactions to pain. So nobody
suspects other people might experience pain as pleasure and vice versa. Obviously not!
There are no obvious signs for colour qualia, so it makes sense to suspect some people experience red as blue and vice versa.

Still, there are weak reactions to colours, like sometimes certain colours are associated with certain emotions. But, this is very weak evidence and could easily mismeasured, or be bound up with culture rather than biology.

We could test it: take pairs of identical twins at birth (so that they haven't learned words for colours yet), re-wire optical nerves of one of each pair so that red and blue receptors were switched (and perform a placebo operation on the other one, so they don't know who is who), and see whether there is any statistically significant change in the attitudes to different colours or the like as they grow up.

The experiment has various technological and ethical problems :-) But it could be done in principle, so to me this shows the question isn't meaningless, just that it's hard to find the answer.


How does the brain immediately know when one's thirst has been quenched? The question struck me the other day when I drank a glass of water. I understand that there are at least two conditions under which the brain signals thirst: extracellular thirst, when there's not enough fluid in the blood, and intracellular thirst, when the cells need more water to lower the concentration of osmolites.

However, it takes time for water to enter the bloodstream after it has been ingested, and it spends at least a little while in the stomach.

Why does the sensation of thirst disappear despite the water having not yet made it into my bloodstream?

There are two different aspects to or drivers of thirst, osmolality and hypovolemia, with plasma osmolality elevation being the more potent stimulus of thirst.
As stated by @arboviral (and supported by his link), not a lot is known about the mechanisms of immediate thirst satiety. Much more is known about the mechanisms causing thirst, and the mechanisms of return to normal serum osmolality over 120-180 minutes after rehydration than those immediately satisfying it.

Most of the research on this is old (pre-2000). In one often-cited very small study 1, swallowing and esophageal reflexes (or as the authors termed it, “oropharyngeal metering”) had a significant effect on relief of thirst, that is,

  the act of swallowing helps to regulate the volume of fluid ingested by providing an integrated signal proportional to the cumulative ingested volume.2

Study participants were all mildly dehydrated. One (control) group was allowed to drink ad lib. Another was allowed to drink ad lib but as they did so, the fluid was simultaneous extracted from the stomach by a nasogastric (ng) tube already in place. Interestingly, the difference in the amount of fluid ingested between these two groups (N.B. ad lib) was only 15% (the latter group drank a bit more.) The third group was given fluid by ng tube only.

The very act of swallowing fluid boluses induced satiety. However, plasma arginine vasopressin levels (involved in the regulation of fluid intake) dropped rapidly during the first 5 minutes of drinking in both ad lib groups, but not in those given fluids via ng tube, so it is not only mechanical receptors that are involved in quenching of thirst.

This confirmed an older study which demonstrated the importance of the rapid drop in plasma vasopressin in hydration before major changes in plasma osmolality occurred.3

Given the lack of extensive research and the relative immediacy of thirst suppression, The most likely explanation is a combination of sensory modalities and reflexes (mucosal wetness, temperature of rehydration fluid, mechanicoreceptors in the oropharynx, esophagus, etc.), and some rapid hormonal changes - e.g. in AVP - are responsible for limiting the amount we drink when thirsty.

1 Regulation of fluid intake in dehydrated humans: Role of oropharyngeal stimulation
2 Influence of age on thirst and fluid intake
3 Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans


How can a chromosome translocation in somatic cells lead to disease? Looking at this picture...

(source: nih.gov)

...I get the impression that the part of chromosome is attached to other chromosome, but it is not mutated. When we assume that all genes in the translocated part are intact and can still make mRNA, my question is:

How can a chromosome translocation in somatic cells lead to abnormality or disease?

You have made an incorrect assumption-- that all the genes on both chromosomes necessarily remain intact. It's possible that they do, and the the translocation is harmless.

But the transition point could be within a gene. This would usually lead to that copy of the gene becoming inactive, which can cause diseases just like any other loss-of-function mutation.

Alternately, the translocation can fuse two genes in a pathogenic way. While this might seem fantastically unlikely, the fact that the translocations are non-random means that there are patterns that recur frequently. The BRC-ABL fusion (https://en.wikipedia.org/wiki/Philadelphia_chromosome) is one of the most common causes of childhood leukemia. The fusion protein is constitutively active because the regulatory domain of the original protein has been replaced.

Finally, a translocation could separate a promoter element from the gene it controls, which could cause aberrant expression of that gene. The promoter element could also wind up proximal to a different gene and cause aberrant expression of that gene.


Is there any way to tell if a gene is functional for an individual with only a reference sequence and the individual's sequence of the gene? I have gene sequence of a ton of individuals within a subspecies from cdna and the ncbi IDed sequence as well. Is there any way to tell using just the sequence that the gene for an individual is non-function or only partially functional?

In general, no.  There might be specific cases where you can, like if there is a stop codon, or a frameshift mutation early on, or someone else has seen your exact variant and experimentally proved that it has no function.

But in general, you cannot predict function from in silico data alone.


Genomic control explanation I am following the original genomic control article -
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.167.8448&rep=rep1&type=pdf

What's the role of $p_i$ in the article? It says that $p_i$ denotes the frequency of $A_i$ allele in population. Is it derived from Hardy-Weinberg equilibrium?

I would like to know how I should calculate $p_1$ for a specific data set.

I have not read the article but in general the allele frequency is pretty much the easiest statistics to compute from population genetics data.

The allele frequency $p_i$ of the allele $A_i$ is the relative frequency of this allele $A_i$ in the population. In other words, it is the counts of haplotypes having the allele $A_i$ divided by the total number of haplotypes. For the specific case of diploid organisms, this frequency is the count of allele $A_i$ divided by twice the number of individuals.

Consider for example the following data, where we have two alleles in the population, $A$ and $B$. Each individual is denoted by its two haplotypes separated by '|'. For example individual A|B is heterozygous.

A|B A|A A|A A|A B|B A|B A|B A|A A|A A|A A|A A|B A|A A|B

In this population there are $7$ Bs over 14 individuals. That makes a allele frequency for B of $\frac{7}{28} = \frac{1}{4}$.

Of course, if you have genotype frequencies, you could - making a number of assumptions - calculate the allele frequency using Hardy-Weinberg but typically from empirical data, you don't need to go through that.

More information about Hardy-Weinberg rule at the post Solving Hardy Weinberg problems.


Why would low complexity regions be linked with relaxed selection? I'm reading a text (Wagner, 2007) on identifying positive selection. In the paper, the author says that low complexity regions are known to be associated with the relaxed selection. I'm trying to understand why this is true. I get that if the region is under relaxed selection then most mutations would be tolerated but why would that lead to low complexity (other than something like slippage during DNA replication)

It's in the section: "Little overlap between variation clusters and low complexity regions"

Wagner A. 2007. Rapid Detection of Positive Selection in Genes and Genomes Through Variation Clusters. Genetics 176(4): 2451–2463.

Low complexity regions have repeats in nucleotides ( or amino acids ).  E.g.  PPCDPPPPPKDKKKKDDGPP or AAATAAAAAAAATAAAAAAT.  This 2011 article compares 14 individual Plasmodium falciparum genomes and finds that these repeats are highly variable between individuals - some may be short AAAATAAAA  others may be longer AAAATAAAAAAAAATAAAAAAATAAAATAAAA....AATAA even to scores of bases.

I think its not clear what these sequences do, but the mere fact that they can vary so much from one viable individual to another indicates that they are not strongly selective.  *If they were subject to selection, you would be able to see the difference in the variation in the health, fitness, and reproduction that these significant genetic changes have, but in this case the change in sequence would not change the properties of the sequence much if at all. *

I think these are also related to copy number variable (CNV) regions.  which expand and contract in the genome easily even between identical twins.  (sorry for the indirect reference - like many SDN stories, the reference is totally wrong), but I remember this work...


Why isn't there any repulsive force between Na+ and K+ disrupting thier roles in transmembrane voltage/ action potentials Pretty self explanatory question. I have a basic grasp on the "How" and "Why" of Reversal/Action Potential in and between neurons, but this question lingers.

The carriers of the charge are ions and they get repelled from each other well enough. Other than their charge there is only the size in which they differ (for all practical purposes). This means, as long as we are talking about membrane potential, the actors are just a mix of 1+ ions which don't come near each other. When size matters, for example in an ion channel, we are talking about single particles, so there is no action of a repulsive force between K+ and Na+.

From another angle: The charge is a force that emerges from a sea of particles, regardless if they are all of one kind or mixed K+/Na+. If you talk about a force between K+ and Na+ then you would have to separate all 10^15 or so K+ ions from 10^15 or so Na+ ions which is simply impossible, as they are mixed up.

http://en.wikipedia.org/wiki/Brownian_motion

http://en.wikipedia.org/wiki/Ion

http://en.wikipedia.org/wiki/Ion_channel


Insect Egg Case, and if so, What Insect? Observed this object today (early October) in Sabino Canyon, on the north side of Tucson AZ, in a riparian area.  It's attached to a mesquite tree (Prosopis spp).  It's attached to one side of the branch, it does not wrap around the branch.  About 1.5 - 2 cm along the maximum dimension.

Looks like some kind of insect egg case and I'm curious if anyone can confirm and knows the insect.

A local graduate student relayed the answer to me.  It is an ootheca of a praying mantis.  There is some additional background on the egg life history here.  Wikipedia reports there are three mantid species.  The upper-left picture of the ootheca here is essentially what I observed, so we may be looking at the genus Stagmomantis.  There are some other great pics at that last site.


Average number of gene products in (a) eukaryote(s) Due to alternative RNA splicing, it isn't uncommon to ultimately find multiple gene products expressed from one gene in eukaryotes. I'm looking for a reference value for the average number of final gene products expressed per gene for:

... a particular eukaryote (preferably humans).

This can't be too hard to do for one species like humans. I would expect the following formula to provide me with a rough answer. Is this correct?

(number of distinct proteins + numbers of distinct non-translated RNAs) / number of genes

... all eukaryotes as a whole.

This one is slightly more problematic.

One answer can be found in the UniProt FAQ:

  What is the human complete proteome?

  In 2008, a draft of the complete human proteome was released from
  UniProtKB/Swiss-Prot: the approximately 20,000 putative human
  protein-coding genes were represented by one UniProtKB/Swiss-Prot
  entry, tagged with the keyword 'Complete proteome'. This
  UniProtKB/Swiss-Prot complete H. sapiens proteome (manually reviewed)
  can be considered as complete in the sense that it contains one
  representative (canonical) sequence for each currently known human
  gene. Close to 40% of these 20'000 entries contain manually annotated
  alternative isoforms representing over 15'000 additional sequences ...

http://www.uniprot.org/faq/48

So, we have 20,000 genes and 35,000 products yielding about 1.75 gene products per gene. Alternatively, the 8,000 genes undergoing alternative splicing give about 2.88 proteins per gene.


What determines the autumn leaf color? It is autumn out there. Green, brown, red, yellow, and mixed-colored leaves drop from the trees to the ground. What determines the colors of the leaves?

Wikipedia tells me

  Leaf senescence is the cause of autumn leaf color in deciduous trees.

Ok. What does the color code? If a leaf is red, why is it red and not yellow or brown or green or mixed-colored?

There is no color code for the leafs - the color results from biochemical reactions. Basically there are three colors: Green, yellow and red.

Green color is caused by the chlorophyll inside the chloroplasts,
when the leafs are active in photosynthesis.
Yellow color is caused by Carotenoids, which are present in the
leafs all the time, but are masked by the chlorophyll. The
carotenoids become visible when the amount of chlorophyll in the
leafs is reduced, which usually happens in the fall.
The red color is caused by Anthocyanins, which are usually not
present in the leafs. They are made during the late summer and can
also mix up with the carotenoids (color mix) to get intermediate
colors.
Brown color is caused by the cell wall of dry leafs which have no
other color.

For further reading these articles are interesting:

Unravelling the evolution of autumn colours: an interdisciplinary
approach.
The Science of Color in Autumn Leaves

There is also the hypothesis around, that the bright colors are a warning sign to insects, this is called the co-evolution theory of autumn colors. The color should warn the insects that the tree has a high level of defense and thus reduce its parasitory load. You can read more about this hypothesis here:

The coevolution theory of autumn colours.
The shared and separate roles of aposematic (warning) coloration and
the co-evolution hypothesis in defending autumn leaves.


Did toads evolve from frogs? I know frogs still exist but that doesn't mean there wasn't ever a frog population that evolved into toads. Did frogs evolve into toads because their available swamp slowly went away and toads could survive better without water? Did frogs and toads evolve independently from similar selection pressure for shape?

"Toads", as commonly used, are not a monophyletic grouping - that is, all toads do not descend from a single common ancestor which only produced other toads. Instead, it's a polyphyletic grouping of those frog species which show common morphological characteristics related to a primarily terrestrial lifestyle. As a polyphyletic group, the parsimonious assumption is that various species of toads evolved from frogs on multiple occasions.

There's several possibilities for similar morphological features in the different toad lineages. The first is convergent evolution - similar selection pressure in the shared terrestrial environment selected for novel generation of similar features. Another is that the common ancestor of frogs and toads had morphological aspects that were a blend between frogs and toads, and depending on environment "toad-like" or "frog-like" features become more prominent or recessive - that is, "toad" genes are sitting dormant in the DNA of most frog species, waiting for the right environment to be expressed. In all likelihood the true explanation probably will be a combination of the two.

By the way, most toad species still depend on bodies of water, particularly for breeding. For example, the common toad (Bufo bufo) will go to a pond to lay its eggs, where the young toads will spend time as aquatic tadpoles before they metamorphosize into the adult form. So when thinking about toad evolution, it's probably incorrect to view it strictly as frogs compensating for losing access to water (though that might have happened for some species), but rather toads evolving to take advantage of the opportunities presented by a terrestrial habitat that's coexisting alongside watery environments.


Does exercising increase the rate at which UV rays are absorbed and cause affects? Does exercising while in sunlight affect the rate at which the human body absorbs and reacts to UV rays? As sunburn is the secretion of fluids, increased dilation of blood vessels and inflammation of skin would exercising (as it also increases blood vessel dilation for heat loss) accelerate the "sun-burn" process in skin?

The only pathways in which I would see more sensitivity to UV light would be

If you were drenched in sweat and somehow the sweat focused the light/UV.   This is highly unlikely as I don't believe any studies have been done to show that a water based solution causes a more intense sunburn.

(Here is a further explanation by another poster on wetness and sunburn https://physics.stackexchange.com/questions/71263/why-does-wet-skin-sunburn-faster )

The increased dilation of blood vessels results in a more red thus darker and more absorbent skin tone leading to more of a sunburn

Both of these are highly unlikely of increasing the sunburn, so in my opinion exercising shouldn't increase UV absorption or make a sunburn worse. Hope that helps.


Does our heart stop when we sneeze? Is it fact or myth that our heart stops beating for moments when we sneeze? If it is fact, what drives the heart to start beating again?

Both your linked fact from the University of Arkansas

  When you sneeze, the intrathoracic pressure in your body momentarily increases. This will decrease the blood flow back to the heart. The heart compensates for this by changing its regular heart beat momentarily to adjust. However, the electrical activity of the heart does not stop during the sneeze.

...as well as your 'myth' from webMD

  For instance, it's not true that your heart stops when you sneeze. When your chest contracts because of a sneeze, your blood flow is momentarily constricted as well. As a result, the rhythm of your heart may change, but it definitely doesn't stop.

...come to the same conclusion, namely the heart does not stop during a sneeze.


Can plants be grown using lights in the home? Plants need sunlight to grow, mainly the blue and red wavelength of the sunlight . The lights used in homes are also white light, it will also have red and blue wavelength of light.

So , can they be grown in such lights perfectly?

It depends on what kind of light you are using. I recently did an experiment on this for my school's science fair and I found that you can use LED lights to grow plants. Nowadays you can actually buy LED lights called "Grow Lights" to grow your plant and the only difference is that Now the current LED lights that are used include four LED lights into groups where each light can produce the correct wavelength that will allow for increased production of growth. For beneficial growth of the cannabis plant for example  you want to use your LED lights directed at 439nm, 469nm, 642nm and 667nm. Link http://easy420grow.com/what-is-the-difference-between-hid-grow-lights-and-led-grow-lamps


First life forms to evolve controlled flight What was the first living organism able to fly in the skies and control their direction , not just Aeroplankton like bacteria and viruses carried by the winds but something  like an winged  insect or fish  or  something  similar,  and when did it evolve?

It was probably an early Pterygota (winged insect).

To my knowledge, the phylogeny of Pterygota is not completely resolved.

Hennig (1981) describes the following phylogeny

Boudreaux (1987) describes the following phylogeny

Wheeler et al. (2001) offers good evidence for this phylogeny

Odonata encompasses dragonflies and damselflies. Ephemeroptera are commonly called mayflies. The origin of pterygotes was about 300 million years ago.

The very first flying(ish) insect had three pairs of wings (Kukalova-Peck, 2005). The pair present on the first segment of the thorax (counting from the head) was then lost in all extant species. Note however than membracidae are using the developmental pathway for this third pair to make elaborate display (mainly for defence; see below).

Some clades further lost both pairs of wings and one clade, the Diptera (flies) lost only the last pair of wings. This last pair is replaced by halteres that are particularly visible in crane flies (see below)


Pathophysiology of pink frothy sputum in pulmonary edema Pulmonary edema is a condition where fluid leaks into the alveolar spaces. This can be due to to hemodynamic causes like left heart failure and pulmonary venous obstruction or microvascular injury or increased capillary permeability.

Clinically we are taught to differentiate between various types of sputum. The sputum in pulmonary edema is characteristically pink and frothy.

It is important to mention here that the fluid that leaks into the alveolar spaces is a transudate and not blood. Hence it is by no means that the pink is due to blood. Otherwise it would be called hemoptysis.

My question is, why is the sputum pink if blood has no role to play?

Even though the fluid in pulmonary edema is a transudate, there is blood in it. This is substantiated by the fact that there are microhemorrhages in acute lung congestion and hemosiderin laden macrophages or 'heart failure cells' in long standing pulmonary congestion on histology. These signify that RBCs have escaped the vasculature to enter the tissue (and failed to get back to the blood), while the macrophages have consumed them later on.

Since the blood loss isn't very high, the color is pink rather than red as seen in hemoptysis.

The reason for this is likely due to the significant differences in hydrostatic and oncotic pressures when compared with the rest of the body. In the Lung, one edge of the capillary is up against a single, extremely thin alveolar cell that provides very little pressure to counterbalance the increased forces present in pulmonary edema. Without this inward pressure to stabilize the capillary wall, you end up with a situation in which small ruptures occur at weak points in the AC membrane, unlike elsewhere in the body where pressures are more equalized and change is an osmotic process rather than one of cellular disruption.

Although hemosiderin laden macrophages can be a proof that RBCs leave the vasculature, it is important to note that they can be found in other organs too. One example is the chronic venous congestion of the liver, where the hypoxia (due to congestion) can lead to endothelial damage letting out the RBC, which later get engulfed by macrophages.


How does an isotonic environment affect fish? Fish receive oxygen needed from water that passes through their gills. If fish were isotonic to their watery environment, what problems would this pose to them?

Some fish are isotonic to their environment (I read that in some book and they had examples but Google is failing me. Here is a paper instead talking about fish doing well in an isotonic environment). It isn't an issue for getting oxygen; I assume you think that because you think fish get oxygen via osmotic pressure, but "isotonic" (and "hypotonic" and "hypertonic") refer to the transfer of water via osmosis. A fish that's isotonic with its environment doesn't need to take special measures to avoid its cells swelling or shrinking as water floods in or out of them; it doesn't say anything about which specific solutes are in that water to make it isotonic.

As far as oxygen goes, oxygen is constantly being consumed by the fish's tissues so the diffusion is always going to go in the right direction (unless the water doesn't contain enough oxygen in the first place, in which case fish won't survive). In addition I imagine fish blood contains many molecules that preferentially bind to oxygen in ways that make this process even more efficient.


Are there endoscopic technologies for blood vessels? Endoscopic procedures are used to look inside cavities like intestine, esophagus etc. Is it being used to look inside blood vessels?

Blood is hard to see through, so visualization with a camera isn't used (to my knowledge). However, Intravascular ultrasound can be used, though it is expensive and not all that common. Instead, angiography is usually used, by filling the vessels with a radio-opaque dye

There are also many techniques used to treat vascular conditions, like balloons/stents to open and keep open blocked or partially blocked vessels, or to repair valves. You can read more about Interventional cardiology or minimally invasive procedures.


Can environmental pressures affect genes in one generation? Environmental pressures are the catalyst of evolution. Pushing a species to adapt to changes therein. My question is can these mechanisms cause significant adaptation over one generation(parent-> child). My thinking is the pressure of the equivalent of human trauma in a species(depending on neurological and biochemical makeup of said species) would be enough to induce genetic influence.

If not, what is the minimum theorized timeframe for environmental pressures to act?

Edit: This is not a duplicate, the previous question is about one animal's lifetime

Can environmental pressures affect genes in one generation?

Yes. Environmental pressures that cause a change in allele frequency will always produce changes in a single generation. If the environmental pressure is present for more than one generation, it will affect changes in allele frequency over a longer time span.

I'd encourage you to look at this set of case studies from UC Berkeley's Understanding Evolution

To clarify what "pressure" means in the context of evolution. Selective pressure, or evolutionary pressure, as wikipedia describes it, is anything that changes the reproductive success of an organism. It is, by definition, something that has an effect in one generation. Selective pressure causes organisms with certain heritable characteristics (and certain alleles) to reproduce at a different rate from organisms with other heritable characteristics (other alleles). The pressure selects for certain alleles.

Considering the comments, it sounds like you're describing a disorder (psychological ailment, e.g., PTSD, GAD), which may have a heritable diathesis, and an environment (trauma) that causes the expression of that disorder. To consider that environment to be selective pressure, it would need to be present at a population level and cause individuals with that heritable diathesis to reproduce at a different rate than individuals without it. If it did, you would see changes in allele frequency over one generation. Indeed there is no way for selective pressure to cause a change in allele frequency without it occurring in a single generation.  I'm not aware of any study that has demonstrated this to be the case for any anxiety disorder.


What limits the size of fish compared to marine mammals? The largest extant fish species is the whale shark (Rhincodon typus). With a length of 13 meters and a mass of about 20-30 metric tons, the whale shark is relatively small compared to the largest mammals, blue whales (Balaenoptera musculus, 180 tons) and fin whales (Balaenoptera physalus, 120 tons).

Is there a physical, physiological, or anatomical explanation why fish never reached the size of marine mammals?

Bigger isn't necessarily better, but I was wondering if there is a simple explanation why fish species are so much smaller than marine mammals.

I'd suggest that one factor could be the difficulties of breathing water - it is highly inefficient. The following is a summary of this response to a TREE article.
Fish spend 10-30% of their energy on breathing because it is so inefficient to use gills because diffusion rates are much slower and oxygen is less abundant. Gills grow in proportionate scales to body size, generally for every 100% increase in body size there is a 50-90% increase in gill size. Thus the larger fish species are working on a lesser body mass/gill size ratio so they can't take up oxygen very easily.
From this I'd suggest it is difficult for fish to grow gill systems much larger than those of a whale shark as it would become to inefficient for them thrive. By comparison whales are air breathers so, despite "breathing" (collecting fresh air) less frequently they can get much more oxygen from it.
I'm sure there is more to it but at least this is a starting idea. If anyone has more then feel free to add to/edit this answer, I merely suggest this as one possible theory and it is not my field.


How can fruit flies and mice share the same gene that says to build an eye if they evolved separately? I saw a documentary where they inserted the gene of a mouse that basically is the starting "build an eye" command into a fruit fly, and a fruit fly eye grew. My question is, if eyes of different types of animal had different evolutionary beginnings (I don't know much about arthropod eye evolution, but for a different example, as I understand it, cephalopod eyes evolved from skin cells while vertebrate eyes evolved from brain cells), then how is it that the same gene controls the growth of two such evolutionary different eyes?

Both fruit flies (Drosophila) and mice (Mus) are classified  under Bilateria.
The presence of such a highly conserved sequence in both species suggests that they share a urbilaterian ancestor who also used a similar gene to turn on eye formation (not create the whole eye, just start the process).

Even though the structure of insect and mammalian eyes diverged evolutionarily after the common ancestor, the switch that starts eye development worked so well there was little need to change it.  I suppose one could say that it remains backwards compatible.


Are the number of base pairs in a given chromosome same between different individuals? This is a basic question but I couldn't find an answer through a web search; hopefully this is the right place to ask. Is the number of base pairs in a
particular chromosome the same in all individuals? For example if I take an
X-chromosome from two random humans would I count exactly 155,270,560
base pairs in both cases? or are there mutations that would make one longer than the other? If they're not exactly the same, what's the range in length variation?

Welcome to Biology.SE.

  if I take an X-chromosome from two random humans would I count exactly 155,270,560 base pairs in both cases

No, you would probably not find the exact same number of base pairs because mutations do no only change one nucleotide to another (what we call a substitution) but sometimes add or delete few (or sometimes many) nucleotides.

note, btw that you don't need to take two different individuals, you can just consider the two X chromosomes of a female (or any other pair of chromsom in any gender) and find this difference in the length of chromosomes.

  what's the range in length variation?

Good question (+1)!

Telomere issue

Before I start, I want to make clear that I consider the length of those chromosomes at the moment of conception. Chromosomes will vary in length during the lifetime due to telomere reduction. I will not consider this in the following calculations. Also, some mutations directly introduce (or delete) a large number of nucleotides (transposable elements for example), I am not considering those mutations here, assuming they are rare in comparison to to single insertions and single deletions (this assumption might not hold!). So please really take the following with a grain of salt.

Let's make some messy calculations

In classical theoretical population genetics, we tend to consider mostly substitutions. But I can maybe try to make some extrapolation out of this work if you allow me to make some strong assumptions, use poor estimates of actual true values and using some non-rigorous mathematics! This is going to be ugly and not extremely trustful $\ddot \smile $.

Not explaining why this is true (it is a result coming from Coalescent Theory), the expected number of pairwise differences between two neutral sequences for a diploid population is $E[\pi] = 4\cdot N\cdot \mu$ (quite an impressively simple result), where $N$ is the population size (assuming panmictic population) and $\mu$ is the mutation rate for the whole sequence. Assuming a constant per site mutation rate of $\mu_s = 10^{-9}$. Knowing the length of the sequence of interest (chromosom X) $L ≈ 1.55 \cdot 10^8 $, the mutation rate for the whole sequence is $\mu = L\cdot \mu_s = 0.155$. Let's consider a population size of $N = 5 \cdot 10^7$ (the equations assume a panmictic population so I just took some value that felt more or less reasonable to me much smaller than the actual worldwide population size). Therefore the total number of substitutions should be $E[\pi] = 4 \cdot 5 \cdot 10^7 \cdot 0.155 ≈ 10^7$.

Now, let's assume that only a fraction of $\frac{1}{100}$ of the mutations bring variation in the number of nucleotides, we might want consider the value $\frac{1}{100} \cdot 10^7 = 10^3$. And because a mutation that deletes a nucleotide from a long sequence will rather diminish the number of variant in sequence length that increasing it, let's say that will divide this number by 10!... so I'd say that two typical X chromosome would differ in length by about 100 nucleotides.

I am sure that with some work one can come up with more rigorous calculations and a more accurate expectation. Intuitively, the result of 100 nucleotides doesn't sound totally crazy (it is not 1 nor 10^6 at least).

Also, one could probably use available sequence data to estimate this value.


What effect does a bat's echolocation have on other bats? Bat echolocation is a perceptual system where ultrasonic sounds are emitted specifically to produce echoes. By comparing the outgoing pulse with the returning echoes, the brain and auditory nervous system can produce detailed images of the bat's surroundings. This allows bats to detect, localize, and even classify their prey in complete darkness. – Echolocation, Wikipedia

Furthermore, we read that:

  [ . . . ] these bats contract their middle ear muscles when emitting a call, so they can avoid deafening themselves.

So far, so good. But this gives rise to two questions I've been challenging with. (And unfortunately I seem not to be able to find the correct search terms and I don't get relevant results)

Imagine two bats close together, flying in a distance of, say, 1 meter from each other. As we know, both echolocate in order to perceive the whereabouts of their surroundings. Bat #1 emits ultrasonic waves, but contracts its middle ear muscles so it won't get hurt. I imagine these two bats are close enough to each other for the waves to be harmful to bat #2's hearing as well.

Hence, two problems arise

Either the waves aren't harmful to the other one (I'd love some calculations on this, or hints on how to do some myself) or something's happening to bat #2 that doesn't let the ultrasonic waves damage its hearing. Certainly bat #2 isn't supposed to know when #1 will emit those waves, so what is happening?
Won't the waves bat #1 has emitted affect the waves bat #2 will emit? So, won't this affect bat #2's perception? We've seen many bats flying together in real life with [maybe seemingly] no trouble visualizing the surroundings, so this mustn't be the case, but why?

Bat echolocation is an incredible and complex process. Bats can emit two kinds of ultrasonic signals. One is a short pulse (less than 5 ms long) that sweeps a wide range of frequencies (100 Hz to 25 kHz) and is referred to as a FM sweep, or a broadband signal. The second kind in a constant frequency (CF) and is much longer in duration (5-30 ms) and held at a specific frequency. In addition to the fundamental frequency there are first and second harmonics. This important for depth perception, pursuit of prey, and location of other bats!

Specifically, bats measure distance by comparing the time between emitted sound pulses and its returning echo. Rapid FM sweeps are especially well suited for target distance so the bat can adjust easily and locate the target. Bats can determine angle, size, elevation, azimuth, and velocity/movement of object from these time and frequency differences as well. Now, bats calculate their own velocity using the Doppler shift concept of their own echos. Meaning, when their signals comes back to them, they compare the amplitude of what their ultrasonic sound wave would be if they weren't moving to the received sound and calculate actual velocity off that (it is a very complicated process and I'm trying to simplify it to get to your question).

Ok, now that is the basics of echo location, but back to your question: What happens when there are multiple bats? Well, when you have many ultrasonic waves going at once, it might get confusing about which is your signal. At least that what you would think. Since the bats have such a wide range of frequencies they can vocally create (100 Hz to 25 k Hz), bats usually simply change the range they are vocalizing to prevent wave disruption. If you do get an overlap of waves from bats using the same frequency, you get something similar to Doppler effect where amplitudes are not what expected. Since they are pretty drastic changes (sometimes even canceling out the wave entirely), and a bat can sense if another bat is around them by calculating the size of the objects producing noise, a bat will know this distortion is due to another bat and not the prey. As a result one bat will have to change their frequency range. This has become sort of a dominance game for them as a result. The bats heightens (I think, might be lower) the frequency of their signals until one cannot go any farther. The one with the wider range is considered dominant and rules that frequency range. Neat right! Hope that answered your question!

Sources: http://scitation.aip.org/content/asa/journal/jasa/54/1/10.1121/1.1913559

Behavioral Neurobiology by Thomas Crew copyright 2000 (most of info from this source, great read if interested)


Does sunlight kill rotavirus? Does sunlight Kill Rotavirus? Maybe freezing? Norwalk or similar. Its a practical question for bedding.

According to this study, both a high temperature wash (57C) and full spectrum sunlight will kill rotavirus.

It would appear that a washer with a sanitation cycle (newer models often have a cycle that hits or exceeds 165F) would be your best bet for treating bedding.

See Figure 2.


Why reaginic antibodies are absent in these types of syphilis? According to Textbook of Microbiology and Immunology
2e, Subhash Chandra Parija, pg.no; 375

  These(reaginic) antibodies do not appear in early primary syphilis, latent acquired syphilis of long duration, and late congenital syphilis. Therefore, Venereal Disease Research Laboratory (VDRL) and other tests may show false negative reactions during these conditions.

Isn't latent syphilis detected by presence of reaginic antibodies? Then why is it said that it does not appear in long duration?
Why antibodies are not produced in late congenital syphilis?

To make the diagnosis of syphilis, the most common tests fall in two categories :

Non-specific tests like VDRL test & Rapid Plasma Reagin (RPR) test : those detect antibodies against cardiolipin, present in the treponema but also in our cells.
Specific/treponemal tests like TPPA/TPHA & FTA-ABS : antibodies titers against antigen specific to T. pallidum are  measured.

Non-specific titers decrease when antigenic stimulation ceases : either when syphilis is cured (no more treponema), or in the late stage where the number of bacteria present in non-immune-privileged zone is low (treponema is almost eliminated except in the central nervous system, eyes, testis where it is protected from immune response).

Specific titers fall very slowly if at all, once they are acquired.

Thus in late stage syphilis we get the following : VDRL- TPHA+, a source of confusion since this can also indicate old/cured syphilis.


Does coloring affect the perception of depth? I have a question about the mechanics of human vision which may be as much of a physics question as it is a biology/physiology question. I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"? And if the difference in color is truly what produces the difference in perceived depth, can similar effects be noticed with other color pairs at more familiar distance scales?

But then again, there are a couple of alternative explanations that seem more plausible to me on second thought. A black night sky could just as easily be called a dark sky, and the difference in perceived depth is really more a matter of shading. Then I remembered a night sky has stars of course, and it might be that my mind just wants to place the stars at normal "sky depth", forcing the black backdrop to appear even further away.

(Another related question I've been somewhat curious about: what precisely is the perceived "distance to the sky" as far as our intuitions are concerned?)

Yes, color and shading can certainly affect depth perception, as explained by wikipedia:

  Aerial perspective – Due to light scattering by the atmosphere, objects that are a great distance away have lower luminance contrast and lower color saturation. Due to this, images seem blurry the farther they are away from a person's point of view. In computer graphics, this is often called "distance fog." The foreground has high contrast; the background has low contrast. Objects differing only in their contrast with a background appear to be at different depths. The color of distant objects are also shifted toward the blue end of the spectrum (e.g., distant mountains). Some painters, notably Cézanne, employ "warm" pigments (red, yellow and orange) to bring features forward towards the viewer, and "cool" ones (blue, violet, and blue-green) to indicate the part of a form that curves away from the picture plane.

Here are a few examples:

The above is Manet's "Luncheon on the Grass" - and if you look at it briefly it seems the bathing woman is sort of hovering amidst the trio instead of rinsing herself off in the background. This is because the warmer colors flanked by more saturated greens in the grass around her "pull" her forward into the same space as the rest of the painting. Here, scale is one of the major cues that she should be in the background.

Above is Cezanne's "The Bay" and is an excellent example of how warmer colors (reds, yellows, oranges) are used to add depth when contrasted with cool colors (blues, greens, violets). The image works very well, and that's partially because of the colors chosen. You can almost draw a diagonal line between the warm and cool portions of the painting.

  I noticed that if I try to imagine a clear blue daytime sky contrasted with a clear night sky and ask myself which of the two appears closer, my intuition says the daytime sky appears closer. My next thought was, given that a night sky is mostly black, visually the only difference between the two skies is their color. So why is that I want to "blue" is closer than "black"?

Well, there are many differences between the two! The daytime sky has numerous reference points - the horizon, mountains, clouds, airplanes, nearby buildings, etc. I would bet the reference points are the number one reason you perceive the daytime sky to be closer, as our brain is constantly taking them into account without us thinking about it. There are other cues, too: The daytime sky has a gradient to it - that is, the blue of the sky differs due to the curve of the atmosphere, and gradients increase depth perception with more saturated colors being perceived as closer (as opposed to the edges of the daytime sky, which are often less saturated).

The night sky, on the other hand, is pretty much solid black (if you live in suburban or urban areas). The lack of a gradient or other colors immediately robs the observer of some depth perception, and because of the inky blackness of night the other reference points - the horizon, nearby structures, airplanes, clouds, etc. - can practically disappear, robbing the observer of additional depth perception.


What kind of larve is this? Found in shed on terracotta pot in Northwest Oregon Found this on a terracotta pot in my shed

They look like the nest and pupae of a mud dauber wasp; the black and yellow mud dauber is a common species to your area and elsewhere, though I can't personally identify the species clearly from the larvae themselves they certainly are consistent.

A nice view of the nest building process

These wasps have a characteristic very skinny abdomen, and they pack their nests with spiders before laying an egg there. They aren't typically a bother to people because they don't have any communal nest to defend, except for building nests on troublesome places like airplanes.


Do ants see, have brain? I'm new here and I would like to know if ants can see, I mean with their eyes not with antennas: I was walking around and found an ant specy,  they were reacting when I moved my fingers towards them, as if they were seeing.

I would also to know  do they have a "brain" and what I'm the most fascinated by is how do they find their way?

PS: English is not my local language that's why my vocabulary is limited. Please feel free to correct any mistakes and or improve my words. Thanks

Ants do have eyes, though how well (and even whether) they see depends on the ant. They also have brains.

You aren't wrong to put quotes around "brain" since in many organisms the nervous system isn't as centralized as in vertebrates, and when they do have concentrations of neurons in various places ("ganglia") it isn't always in the head, and the one in the head isn't always significantly larger than the other ones, so it's often hard to call that having a brain. This can be true of many insects:

http://cronodon.com/BioTech/insect_nervous_systems.html

Having said that ants do have a centralized nervous system, with the neurons in the head making a larger percentage of their body than most other insects, i.e. they have brains. It appears social insects tend to have larger brains for their body size, which includes bees and ants.

http://guides.library.harvard.edu/fas/Brains/ants

Ants also have eyes; they're just often too small to see clearly, especially when the ant itself is small and the eyes are the same color as the ant's head. Ants descended from wasp-like ancestors that probably had quite good eyes, like modern wasps and bees do. But ants mostly live on and underground and don't need eyes as much as flying, pollinating insects do, and how well ants can see varies a lot between the species.

Or I'll just quote Wikipedia:

  Like most insects, ants have compound eyes made from numerous tiny lenses attached together. Ant eyes are good for acute movement detection, but do not offer a high resolution image. They also have three small ocelli (simple eyes) on the top of the head that detect light levels and polarization. Compared to vertebrates, most ants have poor-to-mediocre eyesight and a few subterranean species are completely blind. However, some ants, such as Australia's bulldog ant, have excellent vision and are capable of discriminating the distance and size of objects moving nearly a metre away.

And the cite for that latter example:
ATTACK  BEHAVIOUR  AND  DISTANCE  PERCEPTION
IN THE  AUSTRALIAN  BULLDOG  ANT
  MYRMECIA
NIGRICEPS

Those same ants even have color vision it seems. Conversely, African army ants appear to be blind, although even that depends on the caste. From Sociobiology of the hypogaeic army ant Dorylus:

On workers:

  Eyes are either reduced or absent.

On males:

  Army ant males do indeed resemble wasps, having large and robust bodies and well developed eyes and wings

So it's very possible the ants you ran into could see your fingers.


Why do stranded marine mammals die so quickly? Mammals have lungs, so do marine mammals. Nevertheless some marine mammals seem to die rather quickly when they strand on a beach.

As they have lungs and can breath while on land, why do they die so quickly? Not being in water only restricts them from food.

Do they maybe try to get back into the water so rudely that they get hurt by rocks and/or break bones? Pressure difference doesn't seem to be a problem as they can jump out of the water as well.

I was wondering after reading this article on stranded pilot whales that got spot but died rather quickly after.

In the case of whales, I always thought that it was something to do with the fact that they rely upon buoyancy to support their weight and this seems to support that view:

  When whales, including small whales or dolphins become stranded on beaches
  they suffer from the pressure of their own weight on their organs,in the
  water they are weightless.  They also suffer from overheating as they have
  blubber that insulates them in the water and outside of the water causing
  them to overheat.  This is why we place wet towels and cold water on their
  fins and flukes when do they strand to help keep their body temperature
  down.  Unfortunately most stranded whales do not survive once they have
  beached themselves.


How to mark an ant with the least disturbance to the ant and the nest How would one go about marking one or more ants in a nest so as to least disturb the ant and the nest? The goal is to be able to know which ant you marked months, or many years up to a lifespan later, while at the same time have the least influence of the markings on the behavior of the ant and the interaction between the marked and not-marked ants.

For this purpose, people usually paint ants on top of the thorax (not on the head where it can prevent eyes and antenna to function normally, nor on the abdomen where it can block the spiracles and prevent respiration), with a bit of acrylic paint applied with a toothpick. Combination of colors are used to identify individuals.

These techniques are currently being replaced by the use of RFID tags and Flashcodes in science, to automate recordings.