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What is this beetle looking fly creature?
I found this fly in my back garden that looks like a beetle with wings and it hovers.

]1
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What is it?

@Remi.b I did add what environment I found it and where in the world I found it

Did you know that all beetles do have wings, and many of them do fly? I think it's going to be hard to identify based just on that picture, since it is quite blurry, but who knows, there are some masters here. It's almost certainly a beetle of some kind, though.

I got a clear video, shame you can't post videos.

It's slightly frowned upon because StackExchange likes to have everything contained on this site where possible to preserve the content of both questions and answers, but in this case I think it would be fine to link to a youtube video, or some other video service or video-to-gif host. Just if you do so, please don't remove it after you get an answer. If someone is able to answer your question they can put a high quality image in their answer.

It is of course it is difficult to tell exactly from the quality of the image, but with mandibles of that size relative to the body (approx. 20-25% of total length) it is very likely to be a male Stag Beetle Lucanus cervus, the mandibles will grow much larger. The antenna sticking out from the side of the head just in front of the eye matches your photo (note: in the image below it looks like two on each side, but it is just the shadow in the photo)

Picture from Wikimedia commons https://commons.wikimedia.org/wiki/File:Lucanus_cervus_1922.png
They can be found flying at dusk, and are found in the SE of England from late May to August.
If you are looking for a good insect ID book, I can recommend "A comprehensive guide to Insects of Britain & Ireland" by Paul D. Brock, published in 2014


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Chewing and weight loss/gain
I have a burning question. I have read many articles which say that chewing food properly, therefore longer, till you have a liquid-like texture, is causing you to eat less calories. However, it causes you to absorb more nutrients. If you would eat the same amount of food. Would chewing make a difference in your weight gain/loss?

I'm assuming that what they are referring to is really not about chewing more, but rather eating more slowly. There is a lot of research that shows that satiety (not necessarily feeling 'full', but feeling satisfied/no longer hungry) is delayed relative to actual eating, so that if you eat more slowly you tend to feel just as satisfied despite eating less. Therefore, that claim is completely predicated on the assumption that you will not eat the same amount of food by chewing more. They should really be more precise, but vague diet advice seems to sell books/get views.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Propagating errors for percentage reduction
Need a bit of help for this particular problem.
I have three averages collected from three genotypes (A, B, and C) and their associated SD (a, b, and c). A is my control.
I have been asked to represent the data as a percentage reduction as compared to A. How do I propagate my error?
Calculation:

% Reduction for A = (1-A/A)100%
% Reduction for B = (1-B/A)100%
% Reduction for C = (1-C/A)*100%

Thanks a ton!

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Cloning DNA fragment - at least trying to
I`ve been trying to clone a fragment (about 1.6 kb) using pGEM system, unfortunately it was not succesful. Then, I moved to pJET, and guess what? Again, very low transformation efficiency. Now I am moving to pENTR. However, I am think about why I am struggling to clone this fragment.
I have tried to increase insert:vector proportion; plate a higher # of e. coli cells; left my ligation reaction overnight, but nothing is very helpful. Does anyone have any guess or suggestion about it? Does anyone think that the fragment is too long?
Thanks :)

The fragment size itself shouldn't be a problem in principle.
Cloning has many steps, so anything you didn't specifically test could be causing problems. If different vectors are also not the problem, you should probably look at your experimental steps:

One problem can often be residual EtOH from cleanup steps, which will make your ligation and transformation very inefficient.
You should also test your competent cells with another plasmid to be sure, that they are still viable
Have you checked that all fragments run at the correct size on a gel? You might have star-digestion or bound enzymes that cause problems. Additionally you could also check the ligation product on a gel (though you won't be able to use that for transformation), to see if the reaction works correctly

Hi Nicolai, thank you so much for your suggestions! I'll test it! Best regards, Matheus!


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Can we artificially produce a species that would be able to live on Antarctic ice sheet?
Can we artificially produce a multicellular species that would be able to live on Antarctic ice sheet?
By means of genetic engineering, selection etc.
UPDATE
There are organisms, called Watermelon snow or, scientifically Chlamydomonas nivalis, which do exactly that: populate snow. They are not multi-cellular, but eukaryotic (not bacterial), photosynthetic and form extensive colonies. They already populate both Arctica and Antarctica. They prefer snow to ice.

Some bacteria manage to live there, besides the arctic cold that kills most of the other animals.... So, you mean to create an organisation, from that kind of bacteria, or just a colony of some monocytes?

There's plenty of wildlife in Antartica already (wiki > wildlife of Antartica)

I know this is closed, but I just want to mention one of my favourite papers: https://www.nature.com/nature/journal/v310/n5974/abs/310225a0.html :)


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Rock cod vs grouper
What is the difference between a rock cod and a grouper? The only difference I notice is that grouper seems to be bigger in size. But other than that, they are very similar.

Added wiki links to your post. Adding links to content improve readability for curious and/or competent users, experts and those reviewing your posts.

I do not understand your question. They are phylogenetically speaking very far apart. The only thing they have in common is that they are ray-finned fishes, just like approx. 30000 other fishes.

The rock cods and the Groupers may look similar, but they belong to different "orders" and "families". Moreover here are the differences I mentioned:

ROCK COD

Kingdom:    Animalia
Phylum: Chordata
Class:  Actinopterygii
Order:  Gadiformes
Family: Moridae
Genus:  Lotella
Species:    L. rhacina

GROUPERS

Kingdom:    Animalia
Phylum: Chordata
Class:  Actinopterygii
Order:  Perciformes
Family: Serranidae
I have strong-texted the two differences. You also wrote that besides they look very similar, the Grouper family is slightly bigger in size than the cods. Well, you observation is correct, because the groupers are closely related with sea basses. In fact, sea basses are included to the same family like groupers: The Serranidae. The enlarged size of the groupers is because they have a degree of relativity with basses that as wikipedia says: Bass is a name shared by many species of fish. The term encompasses both freshwater and marine species, all belonging to the large order Perciformes, or perch-like fishes.
This justifies the size and big body weights we notice to the family serranids, like the common grouper.

This answer is adequate as it stands but could be made stronger by adding a simple phylogenetic tree and possibly a summary of key ecological niche differences.


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Human anti animal antibodies issues in blood testing
Do people have to be exposed to animals to get HAMA antibodies? Can these antibodies impact blood tests with false negatives as well as false positives?

Hi Chris, totally understand, my apologies. I have reworded the question to gain some more clarity on the topic in general.

You do not need to be exposed directly to animals to get human anti-mouse (or human anti-animal) antibodies; you can also be exposed to animal products in various ways.

Circulating anti-animal antibodies can arise from iatrogenic and noniatrogenic causes. The former is the result of the normal response of the human immune system to an administered “foreign” protein antigen. Currently available diagnostic and pharmaceutical agents derived from an animal source are extensive and range from rodent immunoglobulins to hormones isolated from fish. In addition, some recombinant proteins are affinity purified on immobilized monoclonal mouse antibody columns, and the possibility exists for some of the mouse monoclonal antibody to detach and copurify with the protein

You can also get anti-animal antibodies from blood transfusions:

Blood transfusion is also associated with an increased incidence of anti-animal antibodies. A study of 2829 participants in a population health survey revealed that 14.4% of the participants who had been transfused were anti-animal positive, compared with 10.4% of the participants who had never received a blood transfusion. This difference was presumably attributable to infusion of preexisting human anti-animal antibody or as a result of infusion of a foreign antigen present in the unit of blood

or through vaccination:

Vaccination against infectious diseases is another route by which animal protein antigens may be inadvertently presented to the immune system and trigger antibody formation. In the US, chick embryo or egg cultures are frequently used in vaccine production, and residual chicken protein may be present in vaccines, whereas in Europe, some vaccines contain rabbit serum, e.g., rubella vaccine in France, and multimicrobial vaccine (Bruschettini vaccine) in Italy

or "unconventional therapies":

The administration of unconventional therapies is also a route to immunization with animal protein. For example, a patient developed anti-rabbit antibodies following injections of “antireticulocytoxique”, which is a lyophilized serum obtained from rabbits injected with homogenates of human bone marrow and spleen and is intended as a tonic to improve senescence and to reduce fatigue and debilitation

Other routes:

Noniatrogenic causes of anti-animal antibodies include maternal transfer across the placenta to the unborn child (37)(38), animal husbandry or the keeping of animals as pets (39), and the transfer of dietary antigens across the gut wall in conditions such as celiac disease (40)(41). Anti-animal antibodies are also more common in multiparous females (36), and a high incidence of human anti-animal antibodies has also been observed in association with certain disease states, e.g., idiopathic cardiomyopathy

All quotes from Human Anti-Animal Antibody Interferences in Immunological Assays, by Larry J. Kricka (1999).

fantastic answer. Thank you for being so comprehensive.


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Are there any trees that prefer to grow on the floor of water bodies but protrude to the air?
Are there any trees that prefer to grow on the floor of water bodies but protrude to the air? Specifically, those that prefer salt water or grow on shallow sea.

Mangrove swamp trees and shrubs immediately spring to mind. There are many species that fall into this category of trees that grow in intertidal and costal locations. They prefer locations where salt and freshwater mix, known as 'brackish water'.

All roots require oxygen and the species that fall into this category have developed roots that protrude above the surface, called pneumatophores.
Photo from http://www.dutchpickle.com/philippines/palawan/sabang-mangrove-forest-palawan.html
Here is an excellent website with more information
http://www.fao.org/docrep/010/ai387e/AI387E06.htm

Mangrove trees even throw up snorkel roots (Pneumatophores) to get to air.


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How can one determine how much of a region flanking an RNA sequence of interest to include in order to look for interfering secondary structures?
I have a set of RNA sequences, and I have been analyzing slices (i.e. target frames) of these sequences in order to determine whether they conform to certain structural criteria. One of these criteria requires that both the target frame of the RNA sequence and its flanking regions have as few secondary structures as possible, i.e. that the RNA nucleotides flanking the slice are as linear as possible.
Using Python and a number of standalone executables, I have been calculating the minimum free energy and optimal structural conformations of the RNA sequences and their flanking regions (see here for more details: http://math.mit.edu/classes/18.417/Slides/rna-prediction-zuker.pdf), but I realized that there is a slight hiccup in my current approach. Namely, I determine the secondary structures of the flanking regions as though they were sequences isolated from my target frame of interest. Now, given that the whole is more than just the sum its parts, I do not know if the secondary structures that are determined when the flanking region is examined on its own versus when the flanking region is examined including either a part or the whole target frame are the same.
Right now my code evaluates 20 nucleotides up and downstream of the target frame as the flanking regions, but should I instead, for example, evaluate 20 nucleotides up and downstream plus some nucleotides of my target frame? Right now, my target frame is 120 nucleotides long, so it might be worthwhile to consider 10 or 20 nucleotides of my target frame that are attached to the flanking regions. But I'm not sure how many nucleotides from my target length should be considered in order for the number of secondary structures to be consistent in the flanking regions. Or is this approach somehow faulty?


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How do we explain the white feathers of an albino peacock?
Peacock feathers are supposed to produce colours by surface structures modulating the light (in addition to the usual absorption/reflection mechanism)... https://en.wikipedia.org/wiki/Structural_coloration
But how does that explain the existence of an albino peacock? https://www.favrify.com/wp-content/uploads/2015/02/peacock1.jpg
Does albino mutation change the physical structure of feathers in addition to the lack of colour pigments?
Does anyone have a close comparison of the physical difference of the albino vs coloured peacock feathers?

@Tytoalba I did search a fair bit on google and visited probably 7-8 websites, but found none which discuss the albino peacock's peculiarity. I am not a biologist, so I don't know the best places for such research (other than googling)... so I am not sure my rigor of research matches your expectation.

'I am not a biologist'- me neither. :) It was just a pointer because Bio website often receives questions that show no prior research(the level is expected to be Google search mostly). Between you can always check Wikipedia, one can find almost anything on Wikipedia. Since it does have mistakes, it is always better to crosscheck. On googling 'White feathers of peacock', the peafowl link showed up, it mentions leucism at the end  of Plumage paragraph.

More specifically this site explains that the black pigment absorbs the incoming light, leaving the iridescence of the feather's fine structure to dominate. Albinos, which lack this light absorbing pigment have white feathers simply as a "reflection" of the white proteinacious content of the unpigmented eather http://www.webexhibits.org/causesofcolor/15C.html

The surface structuresa that are responsible for the structural coloration of peacock feathers are actually barbules and rods made of the very same biopolymer that is responsible for pigmentation in many other animal species, namely melanin. Just as in other animals, melanin is produced in the melanocyte cells which reside in the skin's epidermis. The conditions of albinism or leucism are due to mutations to genes responsible for melanin expression in those cells, or their absence. So although structural coloration is resposible for the colorful peacock feather, it is the same mechanism that leads to colorless feathers as in other animals.
Reference
a Zi, Jian, et al. "Coloration strategies in peacock feathers." Proceedings of the National Academy of Sciences 100.22 (2003): 12576-12578. https://dx.doi.org/10.1073/pnas.2133313100

Although melanin is a polymer of derivatives of tyrosine, and may contain cysteine, it is not a protein. But +1.


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How does a baby deer stand the day it's born?
I know most creatures take time to learn some things.

Birds take some time to fly.
Human beings take some time walk or stand.

But in the case of the deer species, it's different. It can stand the same day it's born. Why is this so?

Some birds (e.g. Robins) cannot do anything but hold their heads up mouth wide open once they hatch, yet other birds (e.g. chickens) can walk and scratch for their own food within hours of hatching. The difference is incubation time. Consider the intrauterine incubation time of most mammals to be very long, humans intermediate, and marsupials very short (they practically have no back legs even.)

It is also worth considering flight is much more complex and precise form a motion. So comparing flight to walking is not a good idea.

@John Is that true? Walking without falling over, especially on 2 legs, is actually quite complex, and depends on a lot more than just the leg muscles. There are several videos that have gone around the internet of Boston Dynamics' walking robots that are really quite amusing and have taken a lot of development to get to that point. Young human toddlers are another amusing population to observe walking.

@BryanKrause It is still nothing compared to flight which is requires all the ballance but with less margin of error and no support. Image if you had to learn to run without ever being able to learn to stand or walk. You must go from nothing to running, becasue anything less and you fall. There is no standing just falling over or running. That is what flight is like.

@BryanKrause consider that all birds learn to stand and walk on two legs before they learn to fly.

@John - Eaglets are a good example of what you're saying here. But really, walking is a very big deal.

@John Even swifts?

@ChrisH sure they learn to walk before they learn to fly. the parent lures them with food, they start with teaching them to walk across the nest for food then try leading them out of the nest, which quickly leads to learning to fly but it starts with walking.  perching birds are not terribly good walkers but they can do it.

@John have the nestlings learn to clamber over each other but their nests aren't exactly spacious, and there's no room to learn to balance.

@John Some species of Megapode birds can fly on the same day they hatch. https://en.wikipedia.org/wiki/Megapode#Behaviour_and_ecology "Similar to other superprecocial birds, they hatch fully feathered and active, already able to fly and live independently from their parents."

@user151841 and they can walk as soon as they hatch, so what is your point?

@John your first comment appears to intimate that flight is a more difficult task for an organism than walking, so while an organism can just grow to walk, they must practice to develop flight skills, or something. That a bird can hatch and then fly goes against your suggestion.

I couldn't stand the day I was born, in fact the whole thing was quite traumatic

@Mike I can't remember the day I was born; I was very young at the time.

@John From observing infants and toddlers, they go from 'cruising' (crawling and moving about with supports) to running to walking. Walking (and standing still) seems more difficult to master than running for some reason (probably to do with the way we balance). 4 legged creatures don't have the balance issue.

@user151841 the can fly within the day, they can walk as soon as they hatch. I only imply that walking is a simpler behavioral process, and poorly compares to flying. An organism can be preprogrammed to do just about anything, I would never claim that flight has to be learned, just that it is a more difficult "programming" if you will, especially in a vertebrate which do not have flight mechanically programmed the way insects can.

If you compare placental mammals in how much time they need to start walking, you'll see that deer are no exception. Humans are an exception.
Hypothesis of Obstetrical Dilemma
The hypothesis of Obstetrical Dilemma states that humans are born premature. We very much think this is because if we were to be born more developed (like other mammals), our big brain would not be able to make its way through the pelvis. Also, bipedalism leads to a narrower pelvis making the passage of the big brain even more problematic. For this reason, human babies are very dependent on the care of their parents for a long time. This hypothesis is called the Obstetrical dilemma (see Rosenberg 1992, Weiner et al. 2008 among many other papers as well as several books such as Ancient Bodies, Modern Lives for example).
Counter arguments to the Hypothesis of Obstetrical Dilemma
Note however that this hypothesis comes with a few potential contradictions, such as the fact that human gestation is no shorter than the gestation of humans' sister species. Indeed, in chimpanzees, for example, gestation lasts 243 days on average against 280 days on average for humans. These counter-arguments can be found in Dunsworth et al. 2012.

Thanks to @MattThrower and @AdamDavis for their helpful comments.

Does this theory have an explanation for the fact that deer gestate for only 201 days, while humans gestate for 280?  Claiming prematurity doesn't seem to make sense given the huge disparity in gestation time, even while accounting for size and energy requirements.

Maybe worth adding that the evolutionary driver for this is not just larger craniums but also bipedal stance, narrowing the gap in the pelvis.

@AdamDavis gestation is not a great measure of development across species, gestation are often timed to coincide with various natural events like particular seasons, some times with built in slowdowns in development. Comparing the newborn to an adult of the species is a better measure.  Chimps are a good example, they have a shorter gestation than humans but are born more developed.

Despite this question having already two good and correct answers, I'd like to write this one just to explain the technical terms — describing what you're asking — mentioned by @jamesqf in his answer (last paragraph).
Mammal and bird (but also other groups) offspring can be classified as altricial  or precocial. In a very simplified way:

Altricial: A not very (to a certain degree) developed youngling, incapable of taking care of itself. Common examples among mammals are humans (see below), rats, cats, dogs and marsupials. Common examples among birds are the passerine, all of which are altricial.
Precocial: Very (to a certain degree) developed youngling, active, mobile, capable of taking care of itself (mainly regarding locomotion: it doesn't mean the newborn is independent). Common examples among mammals are deer (as you said), horses, cattle, pigs, elephants etc. and, among birds, chickens.

Of course, this is a matter of evolutionary strategy, but it's interesting to understand some constraints. Cetaceans, for instance, have to be precocial, otherwise the newborn would drown.
Human classification is a little more complicated. Some authors classify humans as precocial (which is indeed our ancestral condition), like the other apes, because we have generally a single newborn which is born with the eyes open. However, due to the evolution of brain size in the human lineage, human babies are relatively less developed when compared to the other apes, which makes some sources classify humans as altricial.
Finally, you can find semi-precocial and semi-altricial as well, although those are less common terms in the literature. There is also superprecocial, as the birds from the Family Megapodiidae, in which some species are able to fly in the same day they hatch.

Interesting, especially about the Megapodes.  (Until now I thought that was something Terry Pratchett made up.)  I might quibble about precocial young always being able to take care of themselves.  If you look at e.g. horses, they are precocial in that they're able to stand & run soon after birth, but they still nurse for 4-6 months or longer.

Yes, of course. I hope the readers don't take that literally: chimps are precocial, but it takes several years for them to learn how to manipulate tools and obtain their own food, for instance.

Still, I just edited the answer warning about the "taking care of itself".

If you want super superprecocial, a great example is sharks, which start hunting and killing before they're born. https://www.livescience.com/29198-shark-embryos-cannibalize-others.html

Deer are hardly unique in this,  The young of horses, cows, and I suspect most grazing species are able to walk soon after birth.  The reason, of course, is evolutionary: flight is the species mechanism for avoiding predators, so if they weren't able to flee, they would become lunch for some predator.
Other species have gone down an evolutionary route of having their young in some shelter - a nest or den, for instance - and having adults protect them while they're relatively helpless.  (Marsupials take this to an extreme...)  Both strategies obviously work.
You can learn a lot more about this if you search for altricial and precocial species.

That you use the word "learn" in your question leads me to think that you're under a common misconception that people have about biology. It can seem self-evident to us that certain skills, for animals or humans, are necessarily "learned", but often, this isn't the case.
The first thing to note, there are a number of things that humans can learn, which they cannot naturally do,  such as riding a bike, swimming, doing a cartwheel, speaking a second language, etc.
Second, we are most familiar with how humans grow from infancy to adulthood. We interpret infancy and early childhood as a period when a young person learns a number of basic physical skills, such as using their hands, walking, basic co-ordination such as running and catching, learning to speak, etc.
This leads people to assume that physical skills must necessarily be "learned", or practiced with increasing proficiency in order to attain a level of competence.
However certain observations of the natural world provide stark evidence that a number of physical skills, such as walking, swimming, even running and flying, need not necessarily be "learned", but can simply be grown, the same way that a limb or any other part of the body is grown. Yes, neurology and behavior can grow according to genetic pre-programming, just as the rest of the body does.
Consider the blue wildebeest: "calves can stand within an average of six minutes from birth and walk within thirty minutes; they can outrun a hyena within a day." On the plains of Africa, there are very few places to hide from predators. Clearly they are not learning, however, one may define learning, to run in a day.
Lest you think running is an easy skill to grow, and other skills are harder, megapodes birds are capable of flying the same day they hatch.
Once we understand that complex skills such as running and flight can grow, and need not necessarily be learned or practiced to competency by an organism, we then must question what exactly it is what we are witnessing when we see a young animal "learning" a basic motor skill. Is a young child who is learning to walk actually learning, or are we simply watching them grow the ability to walk, over a period of years, the same way their grow their teeth over a similar period? Or perhaps even a little of both, growth and learning?
The difference can be difficult to tease out in a scientific sense.
So let's look at human speech. Surely this is more complex than walking or flying? As adults, we struggle and take years to learn a second language. Children aren't completely fluent until about 5 years old.
But when we really take a look at language ability in children, we see that there is strong evidence that there is a fair amount of growth involved. A good summary of this can be found in Pinker's The Language Instinct:

Pinker attempts to trace the outlines of the language instinct by
  citing his own studies of language acquisition in children, and the
  works of many other linguists and psychologists in multiple fields, as
  well as numerous examples from popular culture. He notes, for
  instance, that specific types of brain damage cause specific
  impairments of language such as Broca's aphasia or Wernicke's aphasia,
  that specific types of grammatical construction are especially hard to
  understand, and that there seems to be a critical period in childhood
  for language development just as there is a critical period for vision
  development in cats. Much of the book refers to Chomsky's concept of a
  universal grammar, a meta-grammar into which all human languages fit.
  Pinker explains that a universal grammar represents specific
  structures in the human brain that recognize the general rules of
  other humans' speech, such as whether the local language places
  adjectives before or after nouns, and begin a specialized and very
  rapid learning process not explainable as reasoning from first
  principles or pure logic. This learning machinery exists only during a
  specific critical period of childhood and is then disassembled for
  thrift, freeing resources in an energy-hungry brain.

So the idea that complex skills, even language, must be learned, is one that should be looked at critically. Considering the evidence that flight and walking can be grown, the next question is how much learning organisms actually do.

We'd have to look at the other side of this to get a reasonable answer, though.  Would an infant human learn to walk if not prompted/trained to do so by adults?  Would they learn language if not exposed to it during the critical development period?

@jamesqf that's true, but these days it's unethical to do that kind of human experimentation. And it's cruel no matter what time period we're talking about. However there have been natural experiments of children raised without language-- Pinker's book goes into this in great detail. It's worth checking out. He sites several lines of evidence, including children not exposed to language, deaf children, creoles and pidgins, and various child-rearing practices in different cultures.

@cell0 please don't edit correct American spelling to correct British spelling. Either are correct and we should stick to the form the author used

On a practical note not previously mentioned: If deer couldn't walk very soon after birth, they would be very vulnerable to predators, as would their parents who would have to remain nearby to take care of them.  This is true for many creatures - even for predators themselves, if you think about it.

But we see a lot of predators who can't walk soon after birth.  Take wolves (or dogs): they're born with eyes closed, not really able to do much beyond squirm around and suckle at first.  They're raised in the shelter of a den: adults bring them food as they're weaned, they gradually learn to hunt &c...

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Are there any studies detailing the overall "-omics" effects of using bleach to synchronise a C. elegans population?
I wasn’t able to find papers detailing the changes in the transcriptome/proteome of C. elegans when synchronised by bleaching vs not-bleaching. Hopefully someone can point me in the right direction!


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What insect is this? (Central Africa)
I live in Africa (DR Congo). Here we have these insects that look like ants. They appear between May and June.
These insects give severe damage if crushed on the skin. They contain something like acid that burns the skin. I saw many people wounded by them.
So I would like to know what these insects are, and whether they can cause death if swallowed? Can someone point me to where I could learn more about them?

PS: There are no forests near where I live.
Edit:

The insects appear at the end of the rain season (April, May)  and right before the dry season (May, June).
Attracted by (neon) light. I think they fly only once then drop their wings (not really sure).
Can be found in homes (houses).
Can burn skin like acid.
It measures approximately 5 - 8 millimeters (not sure. can't find one right now).
Crawls fast with its tail upwards (don't know how to describe else, see image).
Solitary animal.

It is a Rove beetle of the Genus Paederus.
Why Paederus sp.?

They are brightly colored  rove beetles, Coleopterans with short elytra.
Have metallic blue or green-coloured elytra.
Have bright orange or red on the pronotum and basal segments of the abdomen.

There are widely spread on the planet and I found two species of Paederus sp. that are found in East of Africa, together they are called Nairobi flies.

The medical condition it causes is called Paederus dermatitis.

According to Medical and Veterinary Entomology (2009) "At least 20 of the more than 600 species of Paederus beetles have been associated with Paederus dermatitis", even though Paederus beetles do not bite or sting.
This skin irritation results from contact with pederin, a vesicant toxin in the hemolymph of many but not all females in the genus Paederus.
The toxin is manufactured, not by the beetles themselves, but by endosymbiont bacteria, probably some species of Pseudomonas.
Three different genera of rove beetles, all members of the same subtribe Paederina, can cause paederus dermatitis: Paederus, Paederidus, and Megalopaederus.

Pederin

Pederin blocks mitosis at levels as low as 1 ng/ml, by inhibiting protein and DNA synthesis without affecting RNA synthesis, prevents cell division...

This makes it also a potent antitumour agent.

The manufacture of pederin is largely confined to adult female beetles—larvae and males only store pederin acquired maternally (i.e., through eggs) or by ingestion.
It is a contender of the title of most powerful animal toxin.
It is among the most potent animal products known, more so than Latrodectus venom, which is 15 times more potent than cobra venom.
Ingestion can cause severe internal damage and intravenous injection causes death ...

Further Reading:
1. Dermatitis Paederus: About 06 cases occurred in Bun
ia,
Democratic Republic of Congo
2. STUDIES ON THE MECHANISM OF ACTION OF PEDERINE, 1968
References:

 1. Paederus
2. Pederin
3. Paederus dermatitis
4. Encyclopedia of Entomology
5. The Role of Natural Products in Drug Discovery
6. ChEBI

Note: I found the picture in your question is the same as that of Wikipedia's picture of Paederus.

Oh thank you. It think this answers my question. The image was posted by a friend on Facebook so I thought would be better to ask here.

Very nice answer, Tyto alba


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What is the average membrane potential for a neuron?
I'm familiar with the resting membrane potential and other relevant values, but I wondered if there was any research done on the average subthreshold potential of a neuronal membrane over time.

The average subthreshold potential varies greatly with the type of neuron as well as with brain state. In some states, like slow wave sleep in cortex, the membrane potential oscillates between a hyperpolarized (~rest) and depolarized (~threshold) membrane potential. It's far too broad to come up with an "average" value here.


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Where do cockroaches go in the daytime?
Urban parks in North America teem with sizable cockroaches at night. However, in the daytime they are nowhere to be seen. Where do they go?
I know that they tend to avoid light, but how do they go about finding a hiding spot? Do they just throw themselves into any superficial crack and stay still? Do they travel a substantial distance into storm drains, water pipes, tunnels and hollow walls until they are well out of reach of larger animals? Do they have a nest that they return to every night or do they just use whatever hiding spot is nearby?
And specifically for small urban parks, flowerbeds and lawns - do they dig tunnels in the soil? Do they nest in the trees? Or do they simply leave the park and hide in nearby buildings, sewers, and similar human-built structures?
I ask because while it is obvious they must hide somewhere, I have never actually "gotten the drop on" a sleeping or hiding cockroach in a park - or elsewhere - I've only encountered roaches that were scurrying out and about. Some nocturnal insects can be found by for instance flipping over wet rocks or digging up some soil, but cockroaches despite being large and numerous are nowhere to be seen. Are they just really, really good at hiding?

Basically, yes, cockroaches are very good at avoiding detection. Since you linked to the American cockroach (Periplaneta americana), I'll discuss that species in my answer. I've only twice, in my life, seen an actual cockroach. I don't know what parks you're referring to in your question or if it's that common.
By the time you start lifting up a rock or board to look for a cockroach during the day, it will have already sensed you coming and have left.

They spend most of their time in narrow, tight cracks and spaces where surfaces touch them on both sides.
  (Cockroaches from the University of Minnesota)
Cockroaches like to be touched.
  Roaches are thigmotropic, meaning they like feeling something solid in contact with their bodies, preferably on all sides. They seek out cracks and crevices, and will squeeze into spaces that offer them the comfort of a tight fit. And I do mean a tight fit. The small German cockroach can fit into a crack as thin as a dime, while the larger American cockroach will squeeze into a space no thicker than a quarter.
  (10 Fascinating Facts About Cockroaches)

When you understand how thin a crack can be for a cockroach to wedge itself into, you get a better idea how they hide during daylight hours in the outdoors. Many trees have rough bark with enough crevices for them to hide. They could fit in the thin spaces between the bottom of concrete sidewalk pavers and soil, under leaf mulch and many other spaces you may never have noticed before. It takes very little. Best places to look for them in parks would be around trash receptacles where people toss food they didn't finish eating.

This does not provide an answer to the question. To critique or request clarification from an author, leave a comment below their post. - From Review

I bumped the submit button and quickly hit edit to finish.i wasn't sure if the beginning answer went through or not but I guess it has. ;P

Because cockroaches dislike light, they disappear during the daytime to dark places, including the undersides of appliances like stoves and refrigerators, underneath sinks or other installations, near plumbing, inside light switches and behind wall paneling or doorjambs. They also hide in the insides of bookcases or furniture, the folds of drapes or other fabrics, in piles of detritus like old newspapers, paper bags or pet food bags, and in among brooms or mops. Their hiding places are nearly endless, provided they are dark and usually undisturbed.


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Where are all the dead cockroaches?
Major North American cities are full of large cockroaches. Given their numbers and relatively short lifespan, there must be staggering quantities of cockroaches dying in a city every day. However, I never seem to encounter their carcasses in cities.
I notice a fair number of dead roaches indoors, which actually surprises me since you would think that there is more thorough cleaning and pest control indoors vs. city streets. The number of dead roaches I see indoors seems about consistent with the number of live ones.
However, outdoors I see a lot of live roaches, and hardly any dead ones. Most carcasses I notice are mechanically damaged and near heavy traffic areas, so most likely stepped on by someone who was walking by. But what about roaches dying of natural causes (or disease/poison)? Are there animals that scavenge the carcasses very efficiently (ants? birds?)? Do the roaches like to run away and die in isolation? Do they just not die naturally very often, and usually get hunted by a predator?
Note that I am asking specifically about city cockroaches, in mostly concrete areas.

Ants pretty much scavenge everything. I don't know about North America but in India ants do a good job in finishing off dead/semi-dead cockroaches. :P

I have found cockroaches live around places of low temperature, like water reservoir at my place. The huge number of outdoor cockroaches you mention of might live around underground drainage system, far from the the path you commute.

I looked up Wikipedia, according to it they need moisture and not low temperature.

In the big cities of North America (e.g N.Y), the big piles of dirt and moisture attract many hostile animals such as the ones you mentioned: the cockroaches. You should also consider that in the north there is a very common factor that attracts collonies of cockroaches: the low to mediocre temperatures. Moreover, you should reconsider the cleanliness of the sewers. The sewer and the leftovers that exist there are highly nutritional for the cockroaches. That's why you don't see many dead ones on the streets. And where is the start of the sewers? The sewers start from every house. That's why you notice more roaches in the houses than outdoors. They need a place that might provide them the sewer's environment such as the bathrooms, or an other place in the house that has moisture and is mostly dark. Cockroaches live and die to the same place and don't go somewhere else to die. The decay rate outdoors is higher of course, than indoors because every house is cleaner than the roads. With the process of cleaning many factors, such as mites are swept away to the environment.
For the second part of your question:
Outdoors there are many  scavengers and natural predators for the cockroaches. Some of them are: toads, frogs, beetles, geckos, iguanas and birds.  Entomopathogenic fungi have also been identified as lethal to roaches, as their spores attach to insects and kill them within weeks. Cockroaches affected by fungi then pass the parasite on to other cockroaches, and the cycle continues.
Ants prey on some cockroach species, but other roachess actually live with ants in their colonies. These are called myrmecophiles, meaning lovers of ants. They don't seem to offer their hosts anything in return for living with them, and are usually tiny and unobtrusive. Other species - termitophiles - live in similar fashion with termites.
And yes ants are the major factor of dicomposion in nature, because they devour almost anything.
I hope this answered your question, becaused I used very extended research :)

This is a good attempt at an answer! It would even be better (and attract upvotes) if you added some references to the research you used.


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Why is the heart not in the middle of the body?
All mammals that I can think of have a high degree of bilateral symmetry (In fact, almost every animal I can think of is like this).
So why is the human heart not exactly in the middle of the body? An effect of this is that one lung is slightly smaller. Are there any evolutionary theories on why this came to be?

You could ask that about all organs of which there are only 1.

@RichardTingle Not exactly all. The brain, esophagus, nose, and even skin itself all maintain pretty good bilateral symmetry. The stomach, liver, spleen, etc. might make good questions but could get closed as too broad if done all at once.

The reason you think your heart is off-centre is that, when you put your hand on your chest and feel your heart beating, you're actually feeling the blood pulsing through your aorta. Your actual heart is hidden behind your breastbone so you can't feel it.

@DrZ214: It could easily be argued that we really have two brains, in much the same way that we have two lungs.   But we only have one liver...

Possible duplicate, https://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally?noredirect=1&lq=1

First of all, let me make it clear that the heart is at the vertical centre of the body -- it is not shifted towards left (or right). However, it is slightly tilted towards the left in most cases.

In some cases, it is tilted towards the right, and the condition is called Dextrocardia. For why it is so, lets look at what the heart does. Below is a diagram of double circulation (from here).

As you see, the highest pressure needs to be generated for pumping oxygenated blood into the body. Thus, the left ventricle needs the thickest muscles for this purpose. And due to these extra muscles, the  heart appears extended and seems shifted towards left.
Coming to the evolutionary perspective, it is important to mention that humans are not the only organisms with this feature. Indeed, displacement of the heart towards the left is a conserved feature in all vertebrates (Fishman et al, 1997). See this answer for more information.
Coming to genes, bending of the heart towards one side is actually controlled by the NODAL gene during development. See this diagram (from Jensen et al, 2013):

Tilting occurs in two phases, one during the first four and a half months of intrauterine life and the other, which is actually a 45° rotation to the median plane, later. During the early development of the heart, a process called cardiac looping happens and the straight heart tube develops a bend (see diagram). The NODAL gene, along with the Lefty1 and Lefty2 genes, regulates the speed and direction of cardiomyocyte movement during the development of the heart, leading to this asymmetry. To confirm it, researchers knocked out the spaw/nodal gene from a zebrafish and found randomized development of heart, even symmetric heart, as the result(!) (see Walmsley, 1958 and Rohr et al, 2008).
Now, talking about why this happened in the first place, and why it is so conserved among vertebrates, we need to ask ourselves a basic question: what good would a symmetrical heart be? External symmetry is preferred (probably) because it helps in locomotion; it would be quite difficult to move with your two legs placed away from your center of gravity. But when we talk about internal symmetry, conditions drastically change. We get a major restrictive factor here: space. And limited space always dominates other factors. Seeing that the structure of the heart is necessarily pointed towards one side, it becomes difficult to make it symmetrical. (The only option IMO is to have another pointed end at the right side.) In this case again, what advantage would a symmetrical heart provide? None. And it might even be harmful since having an even bigger heart would mean making both lungs smaller. Thus, a symmetrical heart would only prove to be a liability rather than an asset. See this question for more information.

This is a pretty amazing answer, even giving detail of heart development in the womb. Thanks! If you ever come across an evolutionary theory explaining this, please come back and link to it.

What is the reason for this extra tilting in humans as opposed to other vertebrates? I get that it is because a higher pressure is required to pump oxygenated blood, but why exactly is this?

@another'Homosapien', how on earth do you know so much about this?

You understood correctly. But for clarity, why is the tilting effect more exaggerated in humans than other vertebrates? My guess is something to do with the amount and thickness of oxygenated blood, but I don't know that much about the subject.

Our bipedal stance would also come into play. the torso is in a vertical position with respect to gravity, as opposed to the regular horizontal, so the pumping would be more difficult against other vertebrates of our size.
How is the poisitioning in the great apes?

After almost 10 years in academic biology, I stumble across this question and learn that the heart is in the middle of the torso. Thanks, my mind is blown (and +1 of course).

@another'Homosapien' considering that all the reasons you mentioned in your answer could be satisfied without breaking bilateral symmetry  if the heart was oriented dorsoventrally  is there any evolutionary reason why the heart is oriented laterally rather than dorso-ventrally ? i understand that symmetry _by itself _ is not a feature that evolution tries to achieve but is there a reason for this anyway? excellent answer by the way......

I guess it is elusive in a way... Just thought there should be a reason since the majority if not all species with a structure similar to humans have the same orientation. Although now that I think of it the size does seem to be a plausible reason. And sure thing.. I'll hold my vote until tomorrow :)

Very good answer. Here is a broader view to show the location almost at the center : from a cnbc article   (feel free to add this into your answer ^^)

"it is not shifted towards left (or right). However, it is slightly tilted towards the left in most cases" - Clearly, the center of mass of the heart is off-center because of that tilt. Sufficiently such that the left lung is smaller than the right, and has a different pattern of vascularization. I do still think it is more centered than most people conceptualize, though, so I agree with the overall point, and your description of the development is excellent, thank you.

I just joined this site to upvote this answer. Amazing answer! Thanks for this information. I wish I could give 1k upvotes to this answer.

@bryankrause yeah, certainly it is not in exact middle if you see it from average mass, but also certainly it is not off-center if you see it anatomically...there can certainly be confusion about this ;)

To confirm it, researchers knocked out this gene from a zebrafish and found a symmetric heart as the result(!) (see Walmsley, 1958). You've cited the wrong article...

And due to these extra muscles, the heart becomes a little tilted towards the left. Do you have some kind of reference for this statement? The asymmetric nature of the heart seems more a happenstance of development that doesn't require, nor even warrant, such an explanation.

What is the article? 1958 is well before any knowledge of developmental genes. 2) My point is that even if the ventricles were the same size, the heart would still be on the left side.

@canadianer 1. I'll look for it then ;) 2. Well...the bigger size of LV definitely does contribute to the appearance. I mean, just crop the bottom right part of a heart's image and paste it at bottom left...would definitely look different. Now, lets remove these comments now, for obvious reasons :P

Now this is an answer that goes to the heart of the matter. Good job!

1- Bilateral symmetry means two mirror image halves following sagittal section only along a central axis.In animal kingdom there are examples of no symmetry (amoeba) , radial symmetry (jelly fish) , biradial (comb jelly and bilateral (human - though not exhibiting perfect bilateral symmetry because of heart, gall bladder and liver)
     Heart is not symmetrical on account of its functions -the left ventricle is thicker compared to the right).The smaller Left lung could be the result of a varying functional load associated with oxygenation of the blood.


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Why do sea mammals die on land, and drown on sea?
It's quite confusing to me, why do sea mammals die on land, but also die from drowning if they couldn't reach the sea surface to breath?
Excuse my ignorance but I am really confused!

Did you try finding an answer? (Hint: Respiratory organ of terrestrial vs aquatic mammals?) Questions about elementary biological concepts are considered off-topic if those do not show prior research on Bio Stack Exchange. See this policy to learn more.

@Tytoalba I did search before asking, but google keeps showing results of mass sea mammals deaths.. try yourself and see :)

About why they die on land, this question has an answer here.

I believe dehydration, stress, starvation from not being able to move (except for seals and their ilk) and for large mammals, being crushed by their own bodyweight is the issue on land (air being in plentiful supply)

Mammals use lungs as their respiratory system. These animals in the process of evolution left land and started to live in the water, they developed organs that are used to swim. The shape of body also changed to reduce the resistance of water. In spite of all this they didn't developed gills.
Lungs can help in respiration only in air. So the mammals have to come above water in order to take air. You correctly have noticed that these animals die if they can't reach air, i.e. they die of drowning.
But one thing I want to mention is that they don't need to reach land in order to take breath. They just need to swim up to the surface of water for this purpose.
Anyway, I think you got the point. Feel free to ask if you have further confusion on this topic. I shall explain more if needed.

Welcome to Biology.SE! Please add some references to your answer.

Thank you so much for guiding me. I shall surely add some references.


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Is neurogenesis essencial for learning?
So I read that our brain produces 700 new neurons in the hippocampus every day and that if we perform cognitive demanding tasks, eat omega-3 or exercise (other things?) it can produce even more neurons.
What happens with this new neurons? Say I'm learning some new skills, what role do those new neurons play in the process? Is it possible to learn without neurogenesis?
Edit: I'm interested in this topic (eg: brain, hippocampus, learning). Where can I learn about this from the basics? What classes teach this in college?

No, neurogenesis is not necessary for learning (assuming you are talking about adult neurogenesis: of course you need to generate neurons sometime in development to even have a nervous system).
Easily the most-accepted theory for learning and memory is that learning happens by changes in the strength of synapses, the connections between cells. The strengths of these connections are also often referred to as "synaptic weights." The primary mechanisms for this learning are long-term potentiation and the related spike-time dependent plasticity, as well as the guiding principle of Hebbian learning often stated as "cells that fire together, wire together."
Briefly, long-term potentiation or LTP describes the increase in post-synaptic receptors that occurs under certain conditions: this is what increases the efficacy or strength of certain synapses. One of the key conditions is that LTP tends to occur at synapses that causally contribute to making the post-synaptic cell fire.
Adult neurogenesis primarily occurs in a few localized area of the brain (Zhao et al.,
 2008). Although it is possible there is neurogenesis outside of these areas, it has not been demonstrated conclusively and is certainly not sufficient to be necessary for learning in a normal, uninjured adult brain.
Neurons born in the subventricular zone continually replace olfactory receptors, which have a relatively short lifespan, probably evolved due to their constant exposure to all sorts of potentially damaging external compounds entering the nose. These cells do have to undergo some "learning" processes to integrate into existing networks, but that isn't what you would colloquially think of as learning in general.
The best candidates for cells that actually impact learning to some degree are the new neurons born in the subgranular zone of the dentate gyrus in the hippocampus. The hippocampus is indeed an important structure for certain types of learning, but new neurons aren't necessary for this learning. Although it is still somewhat unclear what the roles are of the new neurons in the dentate gyrus, it is thought that they contribute to the primary roles of the dentate gyrus, which are to help distinguish between similar patterns of activity (Deng et al., 2010), also called "pattern separation."
Two other hypotheses are that adult neurogenesis helps to encode timing information in memories because the new neurons only participate in new memories, or that they allow for incorporation of novel stimuli once the older neurons have been conditioned and tuned only to stimuli that have been experienced before (Aimone, et al., 2013). There is evidence for all of these hypotheses but none of it is conclusive, and all may be true to some degree.
There are many different types of learning and these different types of learning can occur in different brain regions, most of which do not demonstrate any substantial adult neurogenesis. Often people think about associative learning with operant or classical conditioning. There is also episodic learning: remembering events that have happened (this is the type most closely associated with the hippocampus, where perhaps neurogenesis plays some role). There is also motor learning, and several types of learning in sensory systems like habituation or sensitization. Therefore, it is important to understand that learning isn't just one thing, and although the mechanisms can be related they are not always the same.
How to learn more: I can tell you about courses at institutions I have been affiliated with, but of course these could vary between schools. Learning and memory is usually at least part of a systems-level undergraduate neuroscience course, which is often the second of two overview courses in neuroscience. The most common time for students to take such a course would be as a second-semester junior or a second-semester first-year graduate student, because there is prerequisite knowledge in physics, chemistry, molecular biology, and physiology. There are also graduate-level courses in the molecular mechanisms of learning and memory, and theoretical neuroscience courses that cover the computational considerations of learning and memory rather than just the biological mechanisms. These types of courses might be available to a senior-level undergraduate as well.
Of course you can also read some of the review papers I have included here and follow the references they cite for original research, as well. The Aimone review is particularly readable and has some very excellent illustrations for a novice, and also extensively covers the regulation of neurogenesis by behavior and environment.
References
Aimone, J. B., Li, Y., Lee, S. W., Clemenson, G. D., Deng, W., & Gage, F. H. (2014). Regulation and function of adult neurogenesis: from genes to cognition. Physiological reviews, 94(4), 991-1026.
Deng, W., Aimone, J. B., & Gage, F. H. (2010). New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory?. Nature Reviews Neuroscience, 11(5), 339-350.
Zhao, C., Deng, W., & Gage, F. H. (2008). Mechanisms and functional implications of adult neurogenesis. Cell, 132(4), 645-660.

Plenty of AI and machine learning frameworks can learn incredibly quickly, yet they have no neurons and some of them make no attempt to mimic neural networks.
If rote memorization (the simplest and crudest form of learning) is considered learning, then you could even argue that a computer "learns" when you install a new program on it.
So the answer to your question is no.
Even if you aren't accepting computer learning as an example, any half-decent immune system can "remember" previously encountered pathogens and this doesn't appear to rely on neurons.

I think it's pretty clear the OP was asking about learning in the brain...


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Kidney failure → Inhibition of Na+/K+ pump → Heart failure
I read in my biology book:

Due to kidney failure, the concentration of K+ in the body increases. This can lead to heart failure too.

But there wasn't any explanation to the mechanism of this phenomenon. So, I took help of the internet, found out about the Na+/K+ pump and its role in muscle contraction on the Wikipedia page.
But, there wasn't any direct mention of the relation between inhibition of Na+/K+ ion pump and kidney failure. After some brainstorming, I hypothesized the following mechanism:
Due to kidney failure, the aldosterone-catalysed mechanism for keeping the Na+ concentration static in bloodstream stops. So, Na+ ions filtrated by the nephron can't go back to the bloodstream, resulting in a decreased concentration of Na+. Then, the decreased potential difference between intra and extracellular space, in terms of Na+ ions, inhibits the Na+/K+ pump. As muscle contraction is dependent on the Na+/K+ pump, heart muscles stop to work.
Is my hypothesis right?

Basically, you are right... But you should really consider and the HUGE role of the Na+/K+ pump on the neurons... If that pump is blocked from high intra consertration of Na or K the pump won't work and as a result the nerval impulse will be deleted. This means that the Autonomic nernous system of the heart will collapse and as a result you will have heart failure. It is like a machine that doesn't get orders.....

@The_Mad_Fish No, this is not right. See my answer below.

@BryanKrause Ok wait to check your answer.

Hyperkalemia (too much blood K+) caused by kidney failure is because the kidney is not clearing excess K+, and most K+ excretion is by the kidneys. Usually kidney failure alone isn't sufficient to cause hyperkalemia (Lehnhardt and Kemper,
 2011), and note that kidney failure can cause problems via many other mechanisms besides hyperkalemia.
The reason that hyperkalemia causes problems with heart and other muscle function isn't directly because of the Na+/K+ pump, but because of how the electrical potential of cells controls contraction. Cardiac myocytes, like most cells, have a negative resting potential, with high K+ inside and low Na+ and Ca2+ inside, and a resting conductance that is higher for K+ than the other ions. When the cell is depolarized to around -40mV, a rush of Na+ and Ca2+ comes in that further depolarizes the cell and also causes the muscle contraction.
Normally, this "action potential" is terminated by opening K+-channels, which returns the cell to a hyperpolarized/resting state by letting K+ ions flow out, ready to fire another action potential and contract again. However, the resting potential is determined by the Goldman equation and depends on the concentration of each ion both inside and outside the cell. The reversal potential for K+ depends on there being a lot of K+ inside the cell, and very little K+ outside the cell. Therefore, it takes a large negative potential to keep K+ in equilibrium. As the K+ concentration outside the cells increases, the equilibrium potential for K+ gets closer to 0 mV. Eventually, cells can't repolarize after contraction and effectively stay in "contraction mode" without relaxing.
Although the Na+/K+ pump is somewhat dependent on the concentrations of Na+/K+, the typical role for that pump is to push K+ ions into cells and pull Na+ ions out. If blood K+ is high, that will not do anything to prevent the Na+/K+ pump from operating, so suppression of that pump is not having any mediating role in this process.
As a side note, KCl is used in lethal injection in the United States as the final drug administered, which stops the heart by causing immediate hyperkalemia.

Your answer describes the hypercalemia state right? Well that's what and I explained but I thought that the Na+/K+ pump would be blocked and as and you say in your post : "When the cell is depolarized to around -40mV, a rush of Na+ and Ca2+ comes in that further depolarizes the cell and also causes the muscle contraction." I ment that upper but I couldn;t describe it, that's why I posted a comment and NOT AN ANSWER. I will +1 your answer cause it shows extended reseach... can you please edit your answer with links of the sites you found facts? Thank you

@The_Mad_Fish I can add some references, sure, but there is nothing here that isn't widely available on wikipedia. I'm a bit confused by your comment though referring to Na+ and Ca2+ coming in to the cell: that mechanism as I describe it does not have anything to do with impairment of the Na+/K+ pump. Yes, if the Na+/K+ pump was impaired that would be a problem, but that is not the only mechanism to interfere with action potential generation.

Ok I understood where the mistake in my hypothesis was. Thank you for the corrections and for the clarifications. :)


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Do we have information on differential reproductive success for many species?
It has been claimed that human males have a successful reproduction rate of about 40%, whereas females have 80%. This leads to the claim that we have about twice as many unique female ancestors as male. My understanding is that this claim is based on looking at the ratio of the number of generations to our most recent female common ancestor and our most recent male one.
Do we have similar data for other species? I'm especially interested in whether there are species where the number of unique male ancestors is greater than the number of female ones. Is a role reversal, like in seahorses, is sufficient to invert the ratio? Does the ratio invert for bees and ants (species where I understand, each female mates with more than one male)?

Interesting question, but note that bees and ants are a very special circumstance where many of the individuals are of non-mating castes; it doesn't make much sense to think about their reproductive success because they aren't really participating in reproduction. My suggestion would be to leave those cases out of your consideration, or only consider the mating individuals.


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What is this fungus that is growing on my plant, and is it dangerous?
This fungus is growing on a plant in my front yard and I do not know if it is dangerous for my health or for the plants health. Can you please identify it? I live in Dominican Republic, a tropical island in the Caribbean Sea.
Here are some photos from my yard:

It is probably not good for the plant by the looks of it. But I think this question should be moved to gardening.se

Looks more like an insect invasion...

Also, please add your location.

My answer won't apply if your plant isn't a cycad (a species from the genus Cycas) as only cycads are affected. Cycad aren't native to the Dominican Republic but have been planted as ornamentals in many parts of the world. If your plant's a cycad, I'm convinced that what your plant has is NOT a fungal but insect infection - something far more serious for your plant but not harmful for you or other people.
Please compare photos provided to make sure of identification. Even enlarging your top photo,  it's not quite focused or clear enough to be sure. It appears that your white 'fungus' is actually Aulacaspis yasumatsui or the Asian cycad scale insect. Athough native to southeast Asia, it's been spreading to many places where cycad are found. Whether it's reached the Dominican Republic yet, I don't know but its been in Florida since the mid-1990s and is found in a number of Caribbean countries. It's now a very serious pest of cycad worldwide, resulting in the death of many.
Here are some photos for you to compare. I did my best to find photos that show greater detail for you to check. If the photos fit what you have, you need to treat your plant to prevent it dying and for the infestation spreading to other cycad on the island. I've no experience with this but the information on how to deal with this pest comes from Central Florida Palm & Cycad Society so they should know the best way to treat this.
Treatment of Asian Scale

 Image from Forestry Images courtesy of Jeffrey W. Lotz

 Image from Central Florida Palm & Cycad Society

Jude as your answer indicate the photos have not been taken you you, in that case the source of the pictures needs to be mentioned. Thank you.

Will do. It's weird but when I answer using my phone, either from Chrome or the SE app, most images from a URL won't load. So I end up downloading the images and posting them that way. Using my tablet, images load fine but I don't always have the tablet charged.


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Plants that are siblings: How does this impact pollination?
A friend has two cherry bushes (prunus tomentosa). Prunus tomentosa is said to be partially self-fertile, but benefits from cross-pollination.
The two cherry bushes set fruit, and so my friend saves me two seeds. I plant the seeds at my house, which is miles away from his, and now have two bushes of my own. They are in bloom.
My cherry bushes are siblings. How will this impact their ability to pollinate?

I've used a specific species in my example, but that doesn't mean the answer needs to be species-specific. An answer about plants in general would be fine.

You might get better results on the gardening site for your specific situation. @Remi.b's answer is good for the general biology but going into all the possibilities might be a little too broad. For example, for apples, it is common to add a granny smith tree since it crosses well with a lot of the other varieties people grow. However, if your friends' two bushes were either self-fertile or cross-fertile enough to set fruit I think you are likely in good shape. Another alternative would be if your friend is willing to give you cuttings from their bushes.

In your case, your two bushes might well be half sib (the pollen might come from different donor) and one (or maybe even both) bush might result from selfing event. In any case, if the species is able to self, I don't see why full sib mating would cause any trouble.
Many species protect themselves from selfing. These plants are said to be self-incompatible. The evolution of the genetic mechanism underlying such self-incompatibility has been highly studied and is fascinating. The wikipedia article offers a good overview.


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Who gives a newly discovered microbe its name?
Assuming a hitherto unknown microbe is found - who gives it its name?

I sthere any reason for your question to be specific to microbes? Whether a microbe or multi-cellular organism is found, the problem is the same. Who name it?

Who name it?

Whoever discovered it. Of course, discovering a new species is not as easy as just taking a picture. One has to provide a very thorough description of the species morphology and eventually argue that it should be considered as a new species and not just as a subspecies or something else. See here for discussion on the definition of a species.

How does the discoverer name it?

If the new species is considered part of an already existing genus, then the author has to keep the genus name. The species name the author chooses is mainly to up himself / herself. Consider for example Macrocarpaea dies-viridis (dies-viridis means "green day") was named like this because the researchers were listening to Greenday when they found it!

I know someone who found the first trilobite in a particular stratum in China and was able to name it Han solo. (https://en.wikipedia.org/wiki/Han_%28trilobite%29)

The person who discovers it. Or, maybe more precisely, the person who tells other people that they discovered it.
Journals and societies may have restrictions or guidelines on how those names are chosen, which certainly has some practical implications for the naming. Here is one example from the Journal of Clinical Microbiology:

For guidelines regarding new names and descriptions of new genera and species, see the articles by Tindall (Int J Syst Bacteriol 49:1309-1312, 1999) and Stackebrandt et al. (Int J Syst Evol Microbiol 52:1043-1047, 2002). To validate new names and/or combinations, authors must submit three copies of their published article to the International Journal of Systematic and Evolutionary Microbiology.
It is recommended that a strain be deposited in at least two recognized culture collections in different countries when that strain is necessary for the description of a new taxon (Int J Syst Evol Microbiol 50:2239-2244, 2000).
Since the classification of fungi is not complete, it is the responsibility of the author to determine the accepted binomial for a given organism. Sources for these names include The Yeasts: a Taxonomic Study, 5th ed. (C. P. Kurtzman , J. W. Fell, and T. Boekhout, ed., Elsevier Science, Amsterdam, Netherlands, 2011), and Dictionary of the Fungi, 10th ed. (P. M. Kirk, P. F. Cannon, D. W. Minter, and J. A. Stalpers, ed., CABI International, Wallingford, Oxfordshire, United Kingdom, 2008); see also http://www.speciesfungorum.org/Names/Fundic.asp.
Names used for viruses should be those approved by the International Committee on Taxonomy of Viruses (ICTV) and reported on the ICTV Virus Taxonomy website. In addition, the recommendations of the ICTV regarding the use of species names should generally be followed: when the entire species is discussed as a taxonomic entity, the species name, as with other taxa, is italic and has the first letter and any proper nouns capitalized (e.g., Tobacco mosaic virus, Murray Valley encephalitis virus). When the behavior or manipulation of individual viruses is discussed, the vernacular (e.g., tobacco mosaic virus, Murray Valley encephalitis virus) should be used. If desired, synonyms may be added parenthetically when the name is first mentioned. Approved generic (or group) and family names may also be used.
Microorganisms, viruses, and plasmids should be given designations consisting of letters and serial numbers. It is generally advisable to include a worker's initials or a descriptive symbol of locale or laboratory, etc., in the designation. Each new strain, mutant, isolate, or derivative should be given a new (serial) designation. This designation should be distinct from those of the genotype and phenotype, and italicized genotypic and phenotypic symbols should not be included. Plasmids are named with a lowercase "p" followed by the designation in uppercase letters and numbers. To avoid the use of the same designation as that of a widely used strain or plasmid, check the designation against a publication database such as Medline.


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What can give rocket salad (Eruca Sativa) a fish smell?
I bought an 'already washed' plastic tray of rocket salad (arugula, or Eruca Sativa) enclosed in a sealed plastic bag. It has been kept in the refrigerator for four days. When I opened it, some 12 days before the "best before" date,  I noticed a strong smell of fish.
I am a regular consumer of this sort of vegetable, I also have some in my garden, so I know how it smells. Yet, by searching on the net I realized that other people have lamented this fish smell in their pre-washed arugula salads.
I am wondering now where does this fish odor come from? Can it come from the plant itself, or is it a side-effect of industrial washing? What exactly is giving this smell? Bacteria, molds, natural decomposition of the plant's essences, or something else?
(Following my instinct I threw the salad away, but I did taste a few leaves and it did not taste 'bad' or 'foul'. It was just the smell that was off.)

A lot of people report a bad smell/taste from arugula when it gets too big, the leaves are best when they are very young. (I don't mean time since picked, I mean time since sprouted) No idea if this is the same thing you are reporting or anything about your source for arugula.

Note: rocket salad is often not Eruca sativa, but some Diplotaxis, because the later growth quicker. My guest it the the water used: it could contains some algea which gives such smell. Days in plastic is an ideal environment (for the few algae in the original water).

Complete guess - the arugula could contain or be decomposing into amine-containing compounds (known to have a fishy smell).
https://en.wikipedia.org/wiki/Amine#Physical_properties

Not a bad guess if you ask me, considering the seeds contain amino acid


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Basener's ceiling and evolution
There is a theorem in the Intelligent Design literature called Basener's ceiling.  It states that all evolutionary algorithms that attempt to optimize some fitness function will eventually reach a plateau where complexity no longer increases.  This is seen in practice when engineers and computer scientists try to use algorithmic forms of evolution.

There are a number of standard models for the evolutionary process of
  mutation and selection as a mathematical dynamical system on a fitness
  space. We apply basic topology and dynamical systems results to prove
  that every such evolutionary dynamical system with a finite spatial
  domain is asymp- totic to a recurrent orbit; to an observer the system
  will appear to repeat a known state infinitely often. In a
  mathematical evolutionary dynamical system driven by increasing
  fitness, the system will reach a point after which there is not
  observable increase in fitness.

Biological evolution is the same as an evolutionary algorithm in the relevant aspects.  It is a search to optimize reproductive fitness, where the fitness function is just the fact of survival or lack thereof.
How then is evolution able to make organisms continually increase in complexity, as history shows, despite Basener's ceiling?

Four quick flaws:
1) Environments are always changing. The fitness space is dynamic, and includes both biological and non-biological players, the former which are also ever-changing. Given a sufficiently stable ecosystem, one would expect an equilibrium among species to develop (though it could be cyclical). However even if the environment stays constant, novel mutations could always increase the fitness of a given species, which could then affect the fitness of all the other species. Also, natural selection is not the only factor that influences evolution, and other factors can add dynamic instability.
2) You are conflating genetic algorithms with evolution. Genetic algorithms use selection to solve a minimization problem and are typically bounded within fairly rigid constraints. They are motivated by biology, not models for biology.
3) You are conflating complexity and fitness. Complexity can be more fit or it can be less fit. Evolution only selects for fitness, not for complexity.
4) Do organisms continually increase in complexity? Depending on how you define it, they may not. Thinking about humans as a "goal" of evolution or something like that is a feature of creationism or intelligent design, not biological evolution. Some of the most successful organisms on Earth in terms of number of individuals or even biomass are some of the simplest.
There may be others as well.

Over time organisms have become more complex.  Why is this not obvious?  We start with the simplest single celled organisms and end up with a huge, diverse phylogenetic tree.  It seems weird that this is the point of contention.

@yters I'm referring to local/recent versus long term. Yes clearly there is more complex life now than when life first started. That doesn't mean that evolution is directed towards complexity, just that more complexity than it started with was advantageous for some individuals. Although the phylogenetic tree is huge, most individual organisms on earth and most of the diversity are still single-cellular.

Just because multicellularity took longer to evolve, for example, doesn't mean it is better. Becoming multicellular was good for some organisms, at some time, so the trait was maintained. Most unicellular organisms at the time the first multicellular organisms were originating stayed unicellular, and their descendants stayed unicellular over billions of generations.

The paper says we should not see this complexity increase, regardless of whether greater complexity is more advantageous or not to some individuals.

Well, that's pretty obviously wrong. Note, you are focusing on just one of the weaknesses I pointed out. The others still apply.

Regarding your first point, the equilibrium you mention is the main point in the paper.  Evolution always pushes a group towards equilibrium, at which point change ceases.  If the environment is chaotic, then the paper claims fitness remains constant and cannot increase.  The only way that constant progress can occur is if the environment guides the evolutionary process to the different levels of complexity.

But change doesn't cease, because organisms continue to mutate, which changes their fitness. In the paper you cite, the big flaw is that 1) Fitness is fixed for a given genotype, and 2) Genotypes are limited to just a couple possibilities. Yes, in that circumstance, you will get an equilibrium. Never in nature do those circumstances occur. Organisms aren't limited to X base pairs, evolution can both change and add or delete base pairs.

By the way, that paper is not at all peer reviewed, and just in glancing at a few of the functions it is laughably incomplete and would not make it to any reputable journal.

Let us continue this discussion in chat.


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Can a new plant grow from half a Succulent leaf?
Succulents like Crassula ovata can be propagated by simply tearing a leaf from the stem and putting it into soil. The leaf will usually grow roots and additional leaves from the calloused wound, and eventually become a full Crassula plant itself.
Now I only have half of a leaf left, the other half got rotten, and dried out. In particular, the part of the leaf that was attached to the mother plant is missing. The remainder is about 3/4" long.

Is it still possible to grow a new plant from just this part of a leaf? Or is it at least necessary that the part of the leaf that was attached to the stem is still present?

Added wiki link to your post. Adding links to content improves readability for curious and/or competent users, experts and those reviewing your posts.

Can you add some detail to the "from my own experiments" bit? I'd like to hear more anyway, but I'm not sure if you mean you successfully propagated from just the calloused part.

Also, while we're waiting for an answer is there any chance you fancy attempting the necessary experiment yourself? There's nothing wrong with answering your own questions and it sounds like you have access to the plant in question :)

After waiting for a while, I am finally able to answer this question myself:
A part of a Crassula leaf is still able to grow roots and new leaves, even if the part that attached the leaf to the mother plant is missing.
I have tried this out myself. I left the half-leaf depicted in the question on top of soil, watered it occasionally, just to keep the soil humid, but not wet. After roughly 5 weeks the leaf grew a first root from the calloused end. For the photo I have flipped the leaf around, to better show the first root.

In the following month, it grew more roots, and after about a month, the first new leaves started to appear.

At this point there is little doubt that a full plant can grow from this, given the right treatment. It is not different any more from full leaves growing new plants.
Update (June 2018): The plant is now 2 inches tall, and doing well.

So nice to see a story with a happy ending!

I was going to ask you to try it yourself, but you beat me to it by telling yourself to do it and actually did it.. Big bravo to your question and your answer. It's posted on the Stack Bio twitter


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Why hasn't there been a serious effort to develop an anti-inflammatory that blocks the responsible genes?
After numerous years of reading about how to disable inflammation and related treatments, it appears that the common existing approaches are fundamentally wrong.
The most popular over-the-counter treatments target cyclooxegenase (COX) - see:
https://en.wikipedia.org/wiki/Paracetamol#Mechanism_of_action
https://en.wikipedia.org/wiki/Aspirin#Mechanism_of_action
https://en.wikipedia.org/wiki/Ibuprofen#Mechanism_of_action
COX inhibitors have been known to have a wide range of side effects (with even more recently reported, I forget what specifically). They are generally weak and only decrease rather than eliminate inflammation completely at the recommended dose.
The common prescription approach is largely topical steroid creams such as hydrocortisone - another crude and bad approach due to increased risk of infection among other side effects
The most recent and promising novel approach appears to be peptide chains that manipulate the immune system:
https://en.wikipedia.org/wiki/Immune-selective_anti-inflammatory_derivative
The main question: Why hasn't there been visible progress on a gene-blocking approach? There are all sorts of ways to block them - find all the proteins and other products that promote or cause inflammation, then consider all sorts of options to stop them. Options including blocking transcription, blocking translation, stopping the protein/product from exiting its cell, blocking its receptor, blocking intermediates.
Future "last resort" treatment for chronic debilitating inflammatory diseases could include "nonsense mutation" gene edits that permanently disable inflammation in specific cell types.
The end result would be a new generation of anti-inflammatory treatment guaranteed to block known mechanisms of inflammation at the source, instead of the largely ineffective and side-effect ridden standard approaches.
The cost might be prohibitive with today's technology although it would almost certainly become feasible with biochemical 3D printing.

Your question is very complex, so for now I'll focus on a few points and answer these first:

Why hasn't there been visible progress on a gene-blocking approach? There are all sorts of ways to block them - find all the proteins and other products that promote or cause inflammation, then consider all sorts of options to stop them. Options including blocking transcription, blocking translation, stopping the protein/product from exiting its cell, blocking its receptor, blocking intermediates.

You are right that all of these options to block genes exist for laboratory or research purposes. Using them on humans as medicine is a lot more complex in a lot of ways though. One main factor I'm not going to discuss much is the cost of all these techniques - which generally a lot more compared to making a simple chemical drug.
Blocking translation
This is a almost a standard experiment for research labs and can usually be done quite specifically (without side effect on most other genes). In oder to achieve a transient (short lasing) effect you usually use RNA knockdown: The introduction of small RNAs, that specifically target the mRNA of the gene you want to knock down, into a given cell with stop transcription in that cells. There are two problems with using this in patients: 1) transformation efficiency: you need to bring RNA into to the cells, which is not a very efficient process. You'll need even higher doses of the stuff to get a strong enough effect in the immune cells you want to target, since it's very hard to specifically target them. 2) The transformation process itself requires either potentially toxic chemicals or viruses to get the RNA into cells, both of which a costly to make and no one wants to take them unless they have to. Taken together this makes RNA knockdown a very bad drug / treatment strategy.
Blocking transcription
The only way to block transcription of a gene permanently is gene editing - which you really don't want to as a short term treatment against inflammation. To make it work transiently you'd have to bring proteins into the cell that bind to and block the genes you want to suppress - inactive transcription factors would do the trick. One (almost minor) problem is that they wouldn't be very specific, so you'd get lots of side effects. The bigger problem is that it's very hard the get a lot of proteins into cells. You'd need large scale transformation and there are many problems with that, which I discussed above.
Stopping the protein/product from exiting its cell
This is an interesting idea, which might actually work - given a few additional years of research. It's probably not possible to this specifically, so you'd generally block the release of proteins from cells. However if you find a drug that only lasts for a few hours it might work. One important caveat is, that the same (or at least a very similar) mechanism is used, when synapses release neurotransmitters - which you definitely do not want to mess with.
There seems to be active research in this area
Blocking its receptor / blocking intermediates
This strategy is very viable in the immune system, where many soluble factors like cytokines with respective receptors are important. Blocking of receptors or soluble proteins can be done by antibodies and there are many people working on this, some antibodies are already licensed by the FDA as drugs for humans. In most cases these are however intended for use in cancer or other more severe diseases, as all of these are immensely expensive.

Future "last resort" treatment for chronic debilitating inflammatory diseases could include "nonsense mutation" gene edits that permanently disable inflammation in specific cell types.

You do not want to this. Inflammation is an important process that keeps your body healthy and permanently disabling it would basically make you immune deficient, which is not a good thing.

The cost might be prohibitive with today's technology although it would almost certainly become feasible with biochemical 3D printing.

Biochemical 3D printing will likely never be a thing. It's possible to print e.g. organs with cells, but printing proteins requires molecular construction and it's unlikely we're ever ging to find a system that's better than what nature came up with during a few million years of evolution.
In general though technological advancements should decrease the cost of all these strategies.

Lots of good answers, some parts are wrong though. You can block DNA -> RNA transcription through obstruction of the promoter or the transcription start site (similar to preventing a file from downloading properly through obstructing the first few bits). Biochemical 3D printing is already in experimental practice - developed at a university somewhere in Illinois a few years back, according to a somewhat old news article. I forget where exactly though.

@user1258361The way to block transcription (which is always DNA-RNA) is excatly what I described, I only didn't specifially mention the promoter. I also know that printing with biochemical materials is possible, but you can't '3D print' a protein.


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Storage of bacteria
Why are strains of bacteria stored when they are inactive (frozen)? What is the problem with storing growing cultures for long periods?

Growing cultures require human care, among other things. Frozen ones require only electricity.

Aside from the comment that frozen cells require less manual maintenance and expense (which is a big plus), active cultures can rearrange/recombine plasmids causing mutations and deletions (especially in the case of toxic inserts). For example, see this article:
Peijnenburg AA, Bron S, Venema G. 1987. Structural plasmid instability in recombination- and repair-deficient strains of Bacillus subtilis. Plasmid 17(2):167-170.

And this is very important. To make experiments comparable and reproducible, you want to be sure you are using the same strain.

Although a bacterial culture on a petri dish, slope or stab culture is in a closed environment and may start healthy, over time, the number of viable cells will decrease to zero as nutrients are being used up. The goal of preserving the cultures in a frozen state is to slow their metabolism and, in relation to that, their death rate so that when the culture is revisited, some of the cells are still viable and available for culturing. The reasons the cells die can be numerous, but in every instance are based on the inherent chemistry of the cells and their environment.  If the deleterious chemical reactions can be slowed or halted, then the overall culture will remain viable for a longer period of time.
As a general rule, the viable storage period of bacteria increases as the storage temperature decreases. Once the temperature is below the freezing point, however, cryoprotectants are essential to reduce cell damage caused by the freezing process.
In addition to the other comments and answers, cryopreservation tubes tend to be much smaller and take up far less space than an agar plate or stab cultures.
Here a table that shows approximate storage spans at different conditions:

Sources:
OPS DIagnostics
Thermo Fisher - Storing Bacterial Samples for Optimal Viability

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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How is the breakdown of lactose regulated at the gene level?
How is the breakdown of lactose regulated at the gene level?
This is my answer: Without lactose in the cell, the repressor protein binds to the operator and prevents the read through of RNA polymerase into the three structural genes. When there is lactose in the cell, lactose binds to the repressor. This causes a structural change in the repressor and it loses its affinity for the operator. Thus, RNA polymerase can then bind to the promoter and transcribe the structural genes.
But I'm not sure if this is right...

Welcome to Bio. Homework questions are warmly welcomed here at Bio, barred you show your research efforts so far. We are not here to simply do the homework for you. If you can provide us with the things you do know, we can fill in the gaps for you. Good luck! I'm putting this question on hold for now. After you've made edits to this post we can re-open it for you. Please don't make another separate question out of it, because then other users cannot see the question history.