text:
Blood become denser when you are dying of deshidration?
Blood become denser when you are dying of deshidration? I mean, when you are dying of deshidration does your body extract water from blood to survie more time?

Your reasoning is a bit off. You need "water" in your blood to survive. When you don't have enough water in your blood, you become thirsty. If you can't drink, water is extracted from your cells to survive. When there's not enough, you die.

Here is an abstract describing an experiment where they kept horses away from water.
Carlson GP, Rumbaugh GE, Harrold D. Am J Vet Res. 1979 Jul;40(7):982-5.
Physiologic alterations in the horse produced by food and water deprivation during periods of high environmental temperatures.

Eight normal horses were held without access to food or water for 72
  hours during a period of high environmental temperatures. During this
  period, the horses had an average weight loss of 51.6 kg (10.7% of
  body weight). Highly significant (P less than 0.001) decreases in
  extracellular fluid volume (18.6 L) and plasma volume (5 L) were
  observed during this period as compared with base-line values. Plasma
  protein, sodium, chloride, and osmolality progressively increased in
  response to the dehydration, whereas packed cell volume, plasma
  potassium, calcium, magnesium, and phosphate were not significantly
  altered. The dehydration and clinicopathologic alterations produced
  were similar to those observed in other species in which the principal
  problem was a water deficit. After the end of the experimental
  dehydration period, the horses replaced 62% of the weight loss during
  a 1-hour period with access to water only.

As the horses became dehydrated they took water from both plasma (the fluid component of blood) and extracellular spaces (tissue water).  "Packed cell volume" refers to red cells.  Red cells and cells in general do not readily give up their intracellular water.  They defend it with osmotically active solutes.  If cells gave up their water the packed cell volume would decrease - like a cup of grapes turning into raisins.
Increase in "Plasma protein, sodium, chloride, and osmolality" reflects to non-water components of blood, which increased in concentration as water was lost.  Like a soup cooking down and getting richer.
This all works the same with humans.

"As the horses became dehydrated they took water from both plasma..." I'm not understanding; how did 'they' 'take water' from plasma? Where did it go to?

@anongoodnurse: To meet their physiologic needs for water.  Ultimately out in urine, sweat, breath and feces.

Urine production stops. Sweat isn't a major problem Breathing is. Feces? They'll stay there and get hard as rocks. I'm not sure where you're getting your info.

@anongoodnurse - if there is any confusion, a fine question for this stack would be "Why do organisms like horses need water?"

I know why animals need water. I'm pointing out that your answer sounds like water in plasma is less important that urine, sweat, breathing and feces. Plasma osmolality increases because there is no external source of water.

Yes blood becomes denser on dehydration (water dilutes the blood, if there's no water in blood it becomes dense). No, body does not draw water from the blood. When you are dehydrated, blood is the first source to be depleted. Then blood pulls water from cells (there are various hormones acting on kidneys and blood vessels trying to preserve the remaining amount of water by increased reabsorption, decreased excretion and vasoconstriction to comparitively useless parts of the body) and on continued dehydration, heart is not getting enough blood to pump as liver is sacrificing all its blood to the brain and cells are being depleted of water and are dried up. So blood is dense and there is not enough amount to reach the brain and brain cells don't get enough glucose (ischemia) and build up of urea and BUN in blood on the other side. Brain Cells switch the metabolism as they try to keep the cells alive only to produce radical oxygen species as by-products which in turn destroys the cells. And hence. Death. Eventually.

It will be very useful if you'll add a few references to your answer.

Umm. You can refer to physiology of brain cells and pathophysiology of Ischemic brain diseases, endocrinology and haematology chapters dealing with excessive excretion of water and body's compensatory mechanisms. I don't want to quote any book titles. You can just refer to any good pathology book. My answer is merely a gist of one of the possibilities of the process and it is related to severe dehydration or medical conditions that are irresponsive despite drinking loads of water. It is more complex than my above explanation. There are so many other pathophysiology of dehydration.


text:
How did genome duplication in jawed vertebrates allow gene specialization?
I am currently reading from Chapter 15 in Principles of Life, 2nd Edition:

Many gene duplications affect only one or a few genes at a time, but in some cases entire genomes may be duplicated. When all the genes are duplicated, there are massive opportunities for new functions to evolve. That is exactly what seems to have happened during the course of vertebrate evolution. The genomes of the jawed vertebrates have four diploid sets of many major genes, which leads biologists to conclude that two genome-wide duplication events occurred in the ancestor of these species. These duplications allowed considerable specialization of individual vertebrate genes, many of which are now highly tissue-specific in their expression.

My question is: how exactly does duplicating a genome enable specialization of genes? In other words, after vertebrates underwent genome duplication, how did one copy of the genome become "highly tissue-specific"?

With a single copy gene, mutations may affect some vital function and are therefore often deleterious and negatively selected. Immediately after a duplication event, there is a level of redundancy in gene function and mutations in one copy giving rise to novel phenotypes are more easily tolerated since the ancestral function is retained by the paralogous gene.
Some reading material, if you feel so inclined:

Wikipedia:
Functional Divergence

Functional divergence is the process by which genes, after gene duplication, shift in function from an ancestral function. Functional divergence can result in either subfunctionalization, where a paralog specializes one of several ancestral functions, or neofunctionalization, where a totally new functional capability evolves.

Neofunctionalization

Following the gene duplication event there are two identical copies of the ancestral gene performing exactly the same function. This redundancy allows one the copies to take on a new function.

Subfunctionalization

Specialization is a unique model of subfunctionalization, in which paralogs divide into various areas of specialty rather than function. In this model both gene copies perform exactly the same ancestral function. For instance, while the ancestral gene may have performed its function in all tissues, developmental stage, and environmental conditions, the paralogous genes become specialists, dividing themselves among different tissues, developmental stages, and environmental conditions.

Kryuchkova-Mostacci N, Robinson-Rechavi M. 2016. Tissue-Specificity of Gene Expression Diverges Slowly between Orthologs, and Rapidly between Paralogs. PLoS Comput Biol 12:e1005274.

The most widely accepted model is that orthologs diverge slower, and that the generation of paralogs through duplication leads to strong divergence and even change of function.

Soria PS, McGary KL, Rokas A. 2014. Functional divergence for every paralog. Mol Biol Evol 31:984-992.

Because genes can be constrained by selection at more than one phenotypic level, the relaxation of constraints following gene duplication allows for functional divergence (FD) along multiple phenotypic axes.

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text:
How does cholesterol affect the fluidity of a plasma membrane?
I was previously taught that cholesterol affects the fluidity of a plasma membrane. At high temperatures, cholesterol decreases fluidity and at low temperatures cholesterol increases fluidity. The Khan academy and Wikipedia pages below say the same thing.
https://www.khanacademy.org/video/cell-membrane-fluidity
https://www.wikiwand.com/en/Membrane_fluidity
Yet, in a current college course, the textbook ("Molecular Biology of the Cell 6th" by Bruce Alberts et al.) says that cholesterol reduces the mobility of the first few CH2 groups of a phospholipid's two fatty acid chains. In this way, the cholesterol makes the lipid bilayer more rigid and decreases the lipid bilayer's permeability to small, water-soluble molecules. However, it says that cholestrol does not actually make the membrane less fluid.
Is the textbook from my current course just a more nuanced explanation, or have I misunderstood something else?

Can you please copy/paste the exact quote? The 4th edition of Alberts clearly says that cholesterol makes the membrane less fluid: "cholesterol tends to make lipid bilayers less fluid at the high concentrations found in most eucaryotic plasma membranes".

Actually, cholesterol has different effects on the fluidity at different temperatures. When it is cold, cholesterol increases fluidity, preventing the membrane from freezing. When it is warmer, cholesterol decreases fluidity.

Lehninger say the same thing. Sterols decrease fluidity

At normal temperatures, cholesterol makes the lipid bi-layer stronger but less fluid because of the way that it forms hydrogen bonds with neighbouring phospholipid and glycolipid heads and fills the space between the bent fatty acid tails. Unfortunately I am still confused about how increasing and decreasing temperature impacts the fluidity.

I've posted a brief answer, but I don't have a link to the Bruce Alberts text to address the specific claim of the CH2 groups.

Cholesterol certainly affects plasma membrane fluidity. In 1978 Cooper found that increasing the ratio of cholesterol to phospholipids decreased the membrane fluidity. This also reduces membrane permeability and reduces the survival of the cells (red blood cells in that case). I imagine this is where the textbooks draw their conclusions.
More recently Rog et al., 2008 demonstrated the importance of the hydroxyl group in the cholesterol by replacing it with a ketone. This affected fluidity and flip flop rate.

In High temperatures, cholesterol stabilises the plasma membrane through raising the melting point, meaning the degree of fluidity is kept the same.
In Low temperatures, cholesterol intercalates between the phospholipid bi-layer and therefore prevents clustering. Clustering is the stiffening of phospholipids (which can be caused by low temperatures) This controls fluidity.
Cholesterol can also decrease the permeability of the cell membrane towards hydrophilic molecules and ions such as Sodium and Hydrogen.

While this is correct, sourcing your information is important.

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text:
What kind of bug did I squish?
I saw a bug swimming through my carpet, and promptly squished it. I had never seen this kind of bug before, and wanted to find out what it is, so that I can assess it's danger to my house and family, and know how to responsibly take care of it. However, my dog gobbled it up before I could take a photograph, so all I have to go by is a mental image:

1.5-2.5 inches long (3-6cm)
2-3 segmented body, with a smaller head, and over 3/4 of it's length was the back segment
Mandibles/Pincers at one end of the body (I can't remember which)
I think it only had 6 or so legs.
The dog made a disgruntled face when she ate it, so I think it could have tasted badly, or bit/stung her tongue as she ate it.
I believe it was two colors, with a pale colored section and a reddish-brown section, although I can't remember their locations.

I live in the Northwestern US, and have three trees on my lot: two maples and a boxelder. The house was built in 1954 and has a crawlspace foundation.

Did it look like this? https://en.wikipedia.org/wiki/Devil%27s_coach_horse_beetle

Or possibly https://en.wikipedia.org/wiki/Earwig?

@arboviral it looked more like an earwig, I'm familiar with those, but it was at least twice as long as any I've seen, and the coloring was different.

Okay; I can't think of anything obvious but if you can add details of the colouring that might help others.

@arboviral -  I've added in what I can remember about color

this i going to be very hard without pictures! some beetle larvae have "pincers" in front, maybe check out some carabid larvae?


text:
Number and function of voltage-independent ion channels
Googling for "voltage-independent" ion channels neurons doesn't give a good overview over the topic (and yields only approx. 50,000 hits, compared to 500,000 hits when searching for "voltage-dependent" ion channels neurons).
What I want to learn:

How many voltage-independent ion channels are there in the brain (or in specific parts of the brain, e.g. cortex) compared to voltage-dependent ion channels? (Rough estimate, order of magnitude: a tenth, a percent, ...?)
Which functional role do they play (compared to voltage-dependent channels which are mainly (?) concerned with the propagation of action potentials along the axon)?

Are there other (and possibly more concise) references than the one I found:
ROLES OF THE ION CHANNEL NALCN IN NEURONAL EXCITABILITY CONTROL (which states, that NALCN is "widely expressed in the nervous system")?
(I guess voltage-independent channels could support the mechanisms of Rall's model which doesn't pressume voltage-dependent ion channels but only modifiable membrane resistances, possibly realized by voltage-independent ion channels, right?)
Addendum: I made a bad mistake not pointing out, that I meant ion channels that are neither voltage- nor ligand-gated but just influence the membrane resistance passively. (Ligand-gated ion channels are of course examples of voltage-independent ion channels, but not the ones I wanted to ask for.) Are the voltage-independent ion channels I wanted to ask for possibly just what is called leak channels?

Yes those would be called leak channels; please don't change your question here though because that would be far to big a change. Note that like in my comment below, the prototypical leak channels (the two-pore-domain potassium channels) are not gated by voltage per se, but they still have some voltage sensitivity.

Those would be referred to simply as 'ion channels'. Voltage-dependent channels should get special mention.
This link from the Blue Brain Project should prove useful:

http://channelpedia.epfl.ch/ionchannels/

A query for 'voltage-dependent' gives me results from 58
channels. According to the original
reference
there should be at least 187 channels in this database (out of the
estimated ~500 ion channels expressed in the brain). That should
give you at least the order of magnitude.
An additional resource can be: https://icg.neurotheory.ox.ac.uk/.
'Non-voltage gated' channels are used to depolarize and
hyperpolarize the membrane. That is as much as specific the answer can be when talking about all of the ion channels. Their specific compartment localization makes a big difference, though. Those that are located in synapses have different functions compared to those that are non-synaptic, for example.
No, voltage-dependent channels are not
solely found in the axon. That is what makes dendrites active
compartments as well. See this very good
review
and my
answer
to
How does a neuron change as you learn?.
In brief, voltage-gated channels facilitate the integration of
inputs on the dendrites independently from the integration at the
level of the soma. This is thought to extent the information
processing capacity of the
neuron.

PS: A lot of your questions suggest that you would be interested in the NEURON simulation environment, as previously suggested to you by @bryan-krause. Using this tool could save you some trouble of trying to re-invent the wheel, as you can start off by using a pre-existing model from ModelDB.

Oops, I seem to have overseen something (what a shame): when did Bryan suggest NEURON to me?

Thanks anyway for your answer, I'll try to follow your advice(s).

First thing I stumbled upon at channelpedia: What does "distributed exponentially" mean? With respect to which variable (distance from soma?), and with positive or negative exponent? (I would guess negative, because channels decrease resistance, thus increase the time constant, thus decrease speed of propagation).

Marginal note: I said "mainly concerned", not "solely concerned".

Nice answer, I have two add-ons: 1) a lot of ion channels, regardless of gating, are made up of multiple subunits. In some cases they are not only heteromultimers, but each protein component can have multiple varieties that can each fit in with the other subunits. Because those subunits are somewhat exchangeable, the number of unique ion channels is quite high, although not all combinations are often observed for various reasons. 2) Lots of channels that are not thought of as voltage-gated still show some voltage dependancy. For example, IRK channels.

Without knowing to what exactly you are referring to, I'd venture to say that they are talking about inter-channel distances, i.e. distances from/to every ion channel's closest neighbour.

Might turn out to be the same.

@vkehayas: I found Bryan's suggestion of NEURON (in his last comment on his answer here: https://biology.stackexchange.com/a/65641/27928)

@Bryan: 1) goes too deeply into details, 2) is more concerned with what we know than how things are.


text:
Where does tracrRNA comes from?
I'm talking about CRISPR system. I know the crRNA is transcribed from the palindromic repeat and the "spacer" but I don't know where the tracrRNA comes from.

Usually the tracrRNA is a part of the CRISPR locus and is encoded in the the vicinity of the CRISPR array (e.g. upstream or downstream of the cas genes or the array).
http://www.genome-engineering.org/crispr/wp-content/uploads/2013/01/crispr_processing1.jpg


text:
What species is this spider?

A friend of mine saw this monstrosity in Taiwan. The photo isn't very clear but you can't blame her considering it was the size of her face. Wanted to know what species it is so I know where they spawn and to stay away from those areas.

I believe this is called Nephila pilipes.
You can refer to Wikipedia for more information

Link only answers are generally discouraged on the stack exchange sites. You can improve the answer by expanding on it.

Not sure how to expand on it. He asked for the name of the species and I answered.

@Casanova You could mention features that make this species identifiable.


text:
Are exosomes useful as a transfection or delivery mechanism in gene editing?
The use of viruses as transfection or delivery agents for gene editing (CRISPR/cas9, etc) is well known. However, one problem with using viruses to deliver DNA into cells is the possibility of triggering an adverse immune response.
Cells already use exosomes to transport various cargo in and out of cells. Does this characteristic make exosomes ideal candidates for delivering gene editing cargo as well?
Also, are there any known examples or studies involving repurposing exosomes for gene editing? Specifically for CRISPER/cas9 applications?


text:
What is this Californian shrub?
I spotted this shrub-like plant in California, USA.

found it in Los Angeles

I'm sure it's listed somewhere within this database. I'm currently categorizing the leaves as: elliptic in shape, pinnate in venation, entire margins. Anyone agree?

@Charles A randomly chosen plant from So. Cal. could be from anywhere given the climate and horticultural practices, so I don't think I'd limit the search to natives.

It may be useful to add a clearer picture of the flowers.

unfortunately i don.t have another picture of it..

Almost definitely not a CA native.
It looks like a coleus to me -- cultivars are pretty diverse but typically have variegated leaves with some amount of purple coloration.
https://en.wikipedia.org/wiki/Plectranthus_scutellarioides

Flowers look very different though...

Not a Coleus. They have square stems and opposing leaves.

It is Bouganvillia. If you have pets you don't want one even if your neighbors have pets. When the flowers drop they get all over the place and if they get into any food or water source for pets they will slowly die from the Poisonous oils that seep out of the flower. Other than that they are a very easy vine to grow and easy to train.

Flowers don't resemble bougainvilla. And leaves don't either as matter of fact.

I know bougainvilla and that wasn.t it.


text:
Are there any techniques for manufacturing exosomes in the lab?
I'm interested in the idea of using exosomes as an alternative transfection agent / delivery mechanism for gene editing applications (CRISPR/cas9, etc).
Information on the matter is sparse.. Does anyone know of any practical techniques for manufacturing exosomes in the lab?

Information on the matter is sparse You can search for any paper that studies exosomes and they'll describe how they obtained them. Is there something specific you cannot find?

"Manufacturing" in the sense of isolation for research or as a clinical product? Current production methods involve multiple ultracentrifugation, filtration and wash steps followed by detection by immunoassay with culture supernatants as a starting material. In other words, you need an ultracentrifuge. There are small-scale kits for exosome isolation but there's a lot of contaminants often times. Try this publication if you can. Wolters-Kluwer/Ovid are hard to access IMO.

@canadianer isolation is not easy for exosomes of certain cell types like cardiomyocytes, where you'd need direct access to a heart. And many cells often only accept exosomes that are specific to those cell types. In light of this problem, it would be desirable to have a way to manufacture or synthesize exosomes tailor made to certain cell types. That's really what I'm looking for. Techniques for synthesis rather than isolation.


text:
single units vs ensemble recording for signal detection
I would like to know, when looking (in vivo electrophysiology) at response properties (latency, magnitude) in response to sensory stimuli, is there any advantage to looking at single units over ensembles of neurons? My ensemble data is really good, while my single units are only ok.
Any advice or resources regarding this would be helpful. I've talked to members of my lab, and looked for answers elsewhere, but havent really found what Im looking for.
Best!

The answer is going to depend a ton on your research question; there can be advantages and disadvantages to each approach.

Can you elaborate please? I am measuring chances in latency of primary visual response to light flashes due to pharmacological manipulations.

First spike latency or similar measures when looking at ensembles only tells you about the latency of the least affected unit when you are talking about latency increases, or the most affected unit when you are talking about decreases.
For example, if you record from 30 cells on a multiunit cluster and the latencies of 29 of them increase but 1 does not change, you might conclude no effect on latency.
Also, changes in detection probability can be harder to recognize in multiunit recordings. If a pharmacological manipulation increases or reduces activity overall, including at distant sites, this might change your threshold of which cells' spikes you can accurately detect as spikes by increasing or decreasing the noise floor.
For example, if your threshold decreases, you might be recording spikes from ~20 cells in your control condition, but then sample from ~50 in your pharmacological manipulation. Note that in this circumstance the total number of spikes you record might actually go down, but you would underestimate the affect because you don't know how many cells you are actually sampling from.
Of course there are problems with single cell recordings too. Sometimes it's really the ensemble activity that matters more, in that case the single units aren't as informative. You also have the problem of tracking accurately a single unit throughout a pharmacological intervention, which can be problematic depending on the time course of the manipulation (electrodes drift, cells die) or if the manipulation itself affects spiking properties (it may be more difficult to ensure you have the same cell if spike widths or amplitudes change).

Thanks a lot for your explaination. I think I'm going to collect single units from the channels I can isolate them on, and ensemble data from the channels I cant isolate single units on. then ill run seperate single unit and ensemble statistics.


text:
What are the advantages using SUMO vector for expression?
My question is : What are the advantages using SUMO vector for expression?

As the pET SUMO info page states

It utilizes a small ubiquitin-related modifier (SUMO) fusion,
  belonging to the growing family of ubiquitin-related proteins, to
  enhance the solubility of expressed fusion proteins.

So, in general, you could consider using SUMO vectors to improve the solubility of your protein.


text:
What is the difference between kingdoms protistae and protoctistae?
I understand that both kingdoms represent primitive eukaryotic organisms, and both contain both unicellular and multicellular organisms.
What are the points that distinguish one kingdom from the other?

First, just a correction: it's "Protista" and "Protoctista", not "Protistae" and "Protoctistae".
They mean the same thing. Those are just different names proposed by different taxonomists for describing the same group of organisms.

Protoctista (or Primigenum) was proposed by John Hogg in 1860.
Protista was proposed by Ernst Haeckel in 1866.

However, as it is common in taxonomy and nomenclature in general, things sometimes get a bit more complicated: some biologists, like Lynn Margulis, don't treat those two terms as synonyms. Particularly, I don't use her nomenclature.

Source:

Jstor.org. (2017). Protozoa, Protista, Protoctista: What's in a Name? on JSTOR. [online] Available at: http://www.jstor.org/stable/4331095 [Accessed 12 Sep. 2017].


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

Related: https://biology.stackexchange.com/q/59205/24354

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

But I have read somewhere (I can't find it) that some monogastric animals (with a one compartment stomach), specially small herbivores animals are able to diggest cellulose with a lesser efficiency than rumians animals. Futhemother cellulase, what another things have them to diggest it without a rumen?

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text:
The insulin protein of apes & chimpanzees
How many amino acids do the insulin protein of apes and chimanpzees compose of?!

Welcome to Biology.SE! There are probably 20-30 extant species of apes (6 of them were sequenced; see here). It will be impossible to answer for every single species. Why do you say apes & chimpanzees. You are interested in all apes but in particular in chimpanzees? Why chimpanzee in particular (why not bonobo, human or a species of gorilla typically)? If you could give some background behind your interest it would be more likely people would find the question worth their time.

Chimpanzees are apes.

On the Ensembl website you can find an easy way to compare genetic sequences of the available genome references, including the one of several primates.
Here a query example:
http://www.ensembl.org/Homo_sapiens/Gene/Compara_Alignments?align=822&db=core&g=ENSG00000254647&r=11%3A2159779-2161341
For protein sequences, check the Uniprot website. For insulin, this is the page you are looking for http://www.uniprot.org/uniprot/P01308
Check the paragraph "Similar proteins", there you will find all the links to retreive the insulin sequence from all the species for which we have sequencing data.


text:
Largest extinct clade?
What is the largest (by large I mean most general) clade of organisms that has gone extinct?
domain > kingdom > phylum > class > order > family > genus > species
So, for example, an extinct kingdom would be larger than an extinct class.

What do you mean by large? Do you mean in terms of number of species, number of individuals, weight of the individuals, ...? Is there any reason why you wrote the taxonomic ranks at the end of your question?

domain > kingdom > phylum > class > order > family > genus > species

added a comment to clear this up

@futurebird those are not clades, those are simply taxonomic ranks of taxa. Not all taxa are clades (most of them, by the way, are not). And, unlike clades, taxonomic ranks are totally, completely arbitrary.

@futurebird There are genuses that contain more species than some classes.

Sometimes an entire phylum has just one species.

I'm not interested in the number of species, I'm interested in extinct creatures most genetically distant from everything alive today.

Semantics aside, I think the OP wants a group of animals which are  grouped together as related and which are extinct.  I propose trilobites.  They are no more but at one time they ruled the earth.
from https://en.wikipedia.org/wiki/Trilobite

Trilobites ( /ˈtraɪləˌbaɪt, ˈtrɪ-, -loʊ-/;[2][3] meaning "three
  lobes") are a fossil group of extinct marine arachnomorph arthropods
  that form the class Trilobita. Trilobites form one of the earliest
  known groups of arthropods. The first appearance of trilobites in the
  fossil record defines the base of the Atdabanian stage of the Early
  Cambrian period (521 million years ago), and they flourished
  throughout the lower Paleozoic era before beginning a drawn-out
  decline to extinction when, during the Devonian, all trilobite orders
  except the Proetids died out. Trilobites disappeared in the mass
  extinction at the end of the Permian about 252 million years ago. The
  trilobites were among the most successful of all early animals,
  roaming the oceans for over 270 million years.[4]


text:
3D Object Modelling in the Brain
Could somebody point out the neuroscience literature dedicated to the modelling of 3D objects in the human mind?
I'm interested in the brain regions, and particularly the details of the circuitry, involved in simulating/manipulating (or planning to manipulate) and/or recognizing 3D objects, or in relating them to the "2D" sensory information. Ultimately, my interest is quantitative, i.e. I'd be especially interested on more computational outlooks on the topic.
Edit: I am aware of the visual recognition pathway, which roughly speaking culminates with the inferior temporal gyrus (in the "what pathway"). However, some animals (not just humans) can simulate object properties (e.g. how will this plastic figurine warp if I bend it a certain way? What is that moving ballerina likely to look like in the next second?). This is more complex than object recognition alone.
Note: my question is asking for pointers to the foundational literature of this topic. I know it's somewhat broad, but I'm essentially asking where to start reading. Thanks! :)

So, you're asking for literary recommendations pertaining to how the human brain senses and interprets 3D objects? If so, me holding a coffee mug, and me seeing the same mug, involve completely different regions of the brain, yet both processes achieve the goal of recognizing the mug to be a 3D object. Given this example alone, I feel that your question yields way too broad of an answer, if one is to be given accurately and wholly. Perhaps you should focus on a single sense..

@Charles Thanks for your comment. I was actually thinking about the modelling of the object, rather than something tied to a specific sense. For instance, the hippocampus and PPC both have multimodal sensory inputs, and encode something involving more than one sense. Although, if I had to choose a sense, I would say vision. I'll also edit to clarify a bit.

Is this the ability you are talking about?
https://en.wikipedia.org/wiki/Spatial_visualization_ability

@futurebird Yes, seemingly so. Though in writing my question I had more of a "simulation" view in mind, e.g. some notion of material properties must be involved when modelling the future.


text:
Effect and functional role of voltage-gated channels on dendrites
I'd like to understand better the effect and functional role of voltage-gated channels on dendrites.
What I believe to have understood:

It is important that a more distal post-synaptical potential (PSP) arrives at roughly the same time and with roughly the same strength at the soma than a more proximal PSP generated at the same time (to give them comparable weights and to detect that they were synchronous). Let me call this the goal of adjustment.
Achieving this goal is the main function of (properly distributed) voltage-independent channels on dendrites (→ Rall model)
The main function of voltage-gated channels on axons is unattenuated signal transport.
Voltage-gated channels on the dendrite lead to non-linearities.

The immediate physical effect of voltage-gated channels on the dendrite is hard for me to imagine and understand. But even harder to understand are the (specific) functional advantages and disadvantages of those channels.
Some possibilities come to mind:

They allow to achieve adjustment better (more precisely) or in some other way more efficiently.
They allow to achieve other goals better or more efficiently (which are only poorly achieved without them).
They allow to achieve completely new goals which are not achievable at all without them (by having some magic computational powers due to non-linearities).
They may have disadvantages (which should not exceed there advantages, otherwise they would not exist), e.g. by distorting PSPs in an unwanted way.

I know that there is a lot of literature on the topic of dendritic processing, but not so many gentle introductions. A gentle introduction - answering some of the following question  - would be welcome. And of course immediate answers!

Do voltage-gated channels on dendrites (distributed as they are) allow to achieve adjustment better or in some other way more efficiently?
Which other goals do they allow to achieve better or more efficiently?
Which new goals do they allow to achieve?
Can their extra computational powers be pinned down?
Which disadvantages do they have (possibly)?

[I believe it wouldn't make sense to split this question into five: they are too strongly related, aren't they?]

As on axons, one immediate effect of voltage-gated channels on dendrites is the generation of spikes (called dendritic spikes as opposed to action potentials). These typically have higher local voltage thresholds than on axons. They seem to play a major role in long-term potentation. But it's not obvious for me how, and which other "implications in neuronal communication, memory, and learning" they might have.

Did you read the review I've suggested to you elsewhere? It is reasonably recent and well-written by two of the authorities in the field. Otherwise, I may be able to conjure a thorough answer when I find the time.

This is also very relevant and written in an accessible way (although behind a paywall).

Sorry, I did not  because it is not free and I don't have access.

Same for both references.

https://www.janelia.org/sites/default/files/Labs/Spruston%20Lab/Stuart_Spruston_2015.pdf
https://pdfs.semanticscholar.org/4890/d678183a2e14a65e5669fc929fe8ddb21a10.pdf
PS: I used google scholar to find PDFs in personal archives

@ykehayas: I finally read the papers (at least substantial parts of them) and found a lot of information I was looking for. Thank you for these great references (which I still have to digest, of course).

I look forward to you supplementing your answer based on your research!

I'll better ask better questions.

Is this one better: https://biology.stackexchange.com/questions/66050/simple-model-of-dendritic-processing?


text:
How can I retain cells in suspension for comparative microscopy?
I am working on a digital holographic microscope. I would like to compare its imaging properties with an actual phase contrast light microscope. My aim is to do this cell by cell, creating a z-stack that shows the same cells in suspension, in a volume with approx. 1-2mm side length. In order to do this, I need to fix each cell firmly in one XYZ position to be able to move them between microscopes.
I am not a trained biologist and I am wondering if there is known procedures/agents to do this. Here's a couple of (non-)requirements I could think of so far:

the cells don't need to live through the process
they should however retain their form for at least couple of minutes (acquisition time)
the agent should be close to translucent and not form bubbles

you can embed the cells in a matrix. You can use agarose, geltrex or fibronectin. I am not sure about their optical properties though.

@alec_djinn Thank you. Someone has pointed me to low-melting-point agarose before.. 600 EUR for 50g though, what in the name of God..

You can use normal agarose as well, it is much cheaper. A 0.5% will do the job.


text:
Red bug with white tips on antennae
These red bugs can be found in hundreds in our locality in Bangalore, India.
They are just about 3.5 cm and have these white (or maybe pale yellow) tips on their antennae.

Can someone identify them and suggest a link where I can find substantial information on their morphology and general behaviour?

What's That Bug? (https://www.whatsthatbug.com/) is another great place to ask for bug identifications.

This question has an answer (previously) already accepted and upvoted. However, the identification is incorrect.
This insect belongs to other Genus, Melamphaus. Here is an image of Melamphaus sp:

The image in the (previously) accepted answer is, in fact, an image of Melamphaus, not Antilochus. What probably happened is that the source (a blog) whose image was copied is wrong. The fact that the blog got the epithet wrong (conqueberti instead of coquebertii) corroborates this.
For comparison, here is an image of Antilochus coquebertii from a reliable source, the Journal of Entomology and Zoology Studies:

Wow... Good job with this correction! +1

I think they are called "Red Bugs" (really), otherwise known as Antilochus conquebertii (aka Antilochus coquebertii).

The black coloring changes from location to location. These were found in India. They were even described by the querent as eating black seeds.
Viet Nam Red Bugs are pretty as well:

The family Pyrrhocoridae is commonly called the Red Bug family, and the family includes the Cotton Stainers as well as the Firebugs, so Red Bugs is the more general family name that includes the other genera and species.

Thank you for the answer but I think it's A.conquebertii, with a double 'i' . Also where can I find some information on them?

@AdDate, Google is your friend.

I didn't find much though. I want some more details.

Antilochus is a sister clade of Pyrrhocoris which we call "fire bugs" (or "gendarme" in french). You'll easily find more info for Pyrrhocoris.

@AdDate Note by the way, that it is more polite to say "I would like" than "I want".

It is also spelled without the "n" in "conquebertii": Antilochus coquebertii.  When I google that name, I get 2000 results, compared to 170 for the other name.  And that is what is used on the (sparse) Wikipedia page: https://en.wikipedia.org/wiki/Antilochus_coquebertii

@BumptiousQBangwhistle - Thanks so much! That is a great help. I'll edit that into my answer.


text:
When did human and animal blood became distinguishable from each other as forensic evidence?
Since a few decades ago, DNA testing became an important tool in criminal forensics, and a lot of information can be gathered from a single drop of blood or from a few cells.
Even before that, blood type could be used even in the early 20th century, to at least exclude 3/4 of possible suspects.
However, when did it first became possible to distinguish between human and animal blood, and what method did they use? Is there information about the first time it was used as evidence in a trial for forensic purposes?
I would suspect it was not sooner, or not much sooner as the discovery of the ABO blood types at the beginning of the 20th century. There are modern, much more accurate methods, and the introductory parts of such papers likely mention the early history, but they are behind paywalls.

Huh. I assumed this would be easy to look up but I've spent a few minutes Googling and come up with nothing. +1!

(Kinda) Related: The Uhlenhuth test (antigen-antibody precipitin test) [ https://en.wikipedia.org/wiki/Uhlenhuth_test ]. You might wanna give the Wiki article on the man himself a read too [https://en.wikipedia.org/wiki/Paul_Uhlenhuth ] ..it's pretty interesting O:)

I'm confused about the "evidence in a trial" part. Are you saying a perpetrator splashed chicken blood at the scene? That a cow committed a crime during which some of her blood was spilled? How would that be relevant in a court of law? In any case, blood of animals often looks different than human blood. In medicine, drug seekers often come in complaining of kidney stones, which are very painful and often require narcotics. The first test for kidney stones is looking for blood in the urine. If it's present, and we think it's trickery, we just look at it under the microscope...

...because they used to carry a bit of blood with them and slip it into the cup while giving a sample. The most common blood (chicken) has nucleated RBC's. Bovine blood  cells (e.g. steak) are unequal in size and have less central pallor. Etc. So I would imagine the first time someone noticed the difference between human and other blood was when microscopes came into widespread use. Now they do something trickier, which I won't elaborate on, to put human blood into the sample, but still easy to catch.

@anongoodnurse : you are right, I had more in mind when it was practical enough to use it in forensics, for example, they find a bloody knife, is it human blood and must they investigate more thoroughly, or can they discard it...


text:
NMDA receptor mediated plasticity figure reference
Because most of this research is over a decade old, finding a paper with a figure that clearly shows that (neuronal) synaptic plasticity (such as long-term potentiation/LTP) is NMDA receptor mediated has proven very difficult for me.
Is there a good reference for this?

Not all types of LTP are NMDA-receptor mediated. To find a paper that shows a form that is, I would suggest searching terms like LTP and NMDA antagonist or blockade or similar.

One of the "Boss references" (nearly 11000 citations right now) for this is Bliss and Collingridge, A Synaptic Model of Memory: Long-Term Potentiation in the Hippocampus.
Being from 1993, it has references to some of the earlier work in this field (if that's what you're looking for).
It notes the different forms of NMDA-dependent and independent plasticity.
Another paper, also from 1993, on this topic is Malenka and Nicoll, NMDA-receptor-dependent synaptic plasticity: multiple forms and mechanisms
Some nice reviews with more recent work, focusing on the NMDAR itself include:

Paoletti et al, NMDA  Receptor Subunit Diversity:
Impact on Receptor Properties,
Synaptic Plasticity and Disease
Lau & Zukin, NMDA Receptor Trafficking in Synaptic Plasticity and Neuropsychiatric Disorders

and their references.

would you directly recommend a figure out of these papers?

@user2305193 What exactly are you hoping for the figure to show?

the NMDA receptor dependency within LTP

@user2305193 How about Malenka and Nicoll's figure 1 (which is actually taken from one of their references)? That shows its dependency experimentally. If you're talking about conceptually, maybe box 2 in Bliss and Collingridge?


text:
Found this spider in my bed last night.. can someone help ID?
As I was going to bed last night, this little guy greeted me when turning the covers. Can someone help ID this for me? I'm located in Kentucky, USA.

Demonstrating size, compared to a bottle cap:

Where are you located?

@canadianer Kentucky, USA. I made the appropriate edit, thanks.

It seems like an Agelenopsis to me. According to www.spiders.us, the size, the description and the location (Kentucky) match your specimen.
Here is another image (also from www.spiders.us), for comparison:

The mentioned link lists 13 species in the Genus Agelenopsis. It shouldn't be difficult narrowing it down to species (if that's the correct Genus, of course).


text:
Which of this 2 affirmations is more close to the explanation of evolution?
I am almost secure that this affirmation aren't exactly true but I want to know which of these statements is more near to a description of how evolution works:

The evolution has an exactly target and always progress to it, each generation the childs are more close to make complete a certain task, that is beacuse evolution is like "directional".
For example: The task is be 10cm taller. Each generation the race become 1mm taller up to complete the task.
The evoultion is random but the specie (or natual selection) try to reach a target, each generation has random traits but only benefical traits tends to "survive" and get offpring.
For example: In order to survive the task is be 10cm taller. Some childs are half cm taller and other childs are half cm smaller, the last ones die naturally and only the taller ones survive enough to get offspring.

This seems like it's some sort of homework assignment, though I am afraid even the better of the two is hardly any better.

One is better but is still awfully unclear, poorly phrased and misleading. I don't feel that if you were to know which one is better, it would not help you much to get basic understanding of evolutionary processes. The best for you is to start with a short and easy intro course such as Understanding Evolution by UC Berkeley for example.

@BryanKrause given how bad the phrasing is, I think we can be clear this not a homework and could answer which one is better, right? So, here we go: The second one is slightly better!

@BryanKrause, that isn't a homework! We don't have biology in school, it's only a curiosity of me.

@Remi.b, sorry for my grammar, english isn't my main language. It's a curiosity that I have, not a homework.

@EnderLook No worries. I am an ESL too and it is not uncommon that other users correct my grammar.

@Remi.b You'd be surprised at the quality of education in some places, especially on evolution...

@BryanKrause Yeah, I agree. For being part of the Evoke community (committee acting on improving education in evolution at all levels in Europe), I also came to realize how poor can be the quality of education in evolution even in countries that normally have good science education (esp. in high school). We have actually already witness a number of very bad homework questions on this site.

@Remi.b This is not a homework (In 5º year of high school we don't have biology)... and I don't live in Europe so I don't think that Evoke would work in my country. Sorry for my poor knowledge about evolution, I was only designing a creature for a ficitonal world whne suddenly I get the curiosity of how that perfect creature (it's to much perfect, too much) could have evolved and then I write the question... sorry.

@EnderLook Don't worry, very few know about Evoke and it really is a side discussion to the post. Bryan and I kind have a side chit chat here (which we probably should not have)!

The second is marginally better because it mentions randomness and emphasizes differential survivorship, but the parts about "trying to reach a target" and specifying a particular "task" are misleading at best. I would rewrite the statement as follows (I have edited for grammar, spelling and style as well, but emphasize more substantive deviations with strikeout for omitted parts and boldface for added parts). The substantive edits change the meaning of the statement significantly: most evolutionary biologists would be very uncomfortable with the second statement as written above (setting aside any grammatical issues).

Evolution is has a random component but the species (or natural selection) tries to reach a target, may result in directional change: each generation has some random variation in traits but only individuals with beneficial traits tends to  are more likely to survive and produce offspring. For example, In order to survive the task is be 10cm taller. taller individuals survive better than smaller ones.  Some offspring are a half cm taller and other children are a half cm smaller; the latter die naturally and only the taller ones survive long enough to produce offspring.

I would probably say "offspring" rather than "children" in a technical context.
Note also that this emphasizes evolution by natural selection; broadly speaking, there are many non-adaptive processes (vicariance, drift ...) that also lead to evolution (change in gene frequencies between generations).

I would remove Evolution is random or maybe jsut edit it to Evolution is partially stochastic or even better Evolution is not a purely/uniquely deterministic process or even Evolution is the results of a number of processes, some of them being deterministic, some being stochastic. Good answer otherwise +1.

Thanks for the answer. Sorry my poor grammar, english isn't my main language.

@EnderLook I just want to clarify for you especially as ESL/ELL, that this answer is correcting more than just grammar.

Don't worry about the grammar, by the way. I modified it because I'm a perfectionist, but there's nothing wrong with trying to express your ideas (my second-best language is much worse than your English).

@BryanKrause, I know, I am no so stupid ;).

@BenBolker, I know, I am not worried about that, I also do the same to other people (but in my main language), about the second-best language... I don't know more language that english and spanish :(.


text:
can dissolving be endothermic process
can dissolving be endothermic process. I have a container with glucose(solid state) and added water and found the container getting colder. was wondering there is no reaction(just a physical process) and why would it absorb heat.

Yes, it can. This a question for [chemistry.se].

The answer to your question in general is yes.
There are many salts and compounds that are endothermic - they cool the solution when they dissolve.  It also turns out that glucose is endothermic when it dissolves if this sheet i found is to be believed.  Its not a strong effect but you made an accurate observation!
Endothermic salts can be quite cold.  This is how home ice cream makers often work in fact - rock salt dissolves into the ice and makes it even colder than it started out to be. I believe that is how ice cream was made before refrigeration and ice storage arrived in the 19th century.

Welcome back! How have you been? How's the company going?

thanks Alice!  very well - raising funds for a new startup...


text:
What attaches plant cells to the cell wall?
In animal cells integrins span the plasma membrane and attach the cell membrane to the extracellular matrix. I was wondering how are plant cells attached to the cell wall? Is it just the middle lamella holding them in place or is there something else (i.e proteins)?


text:
What species is this orange and black caterpillar from Costa Rica?

Does anyone know what type of caterpillar this is? I don't know much about them. Pictured it in January in Costa Rica cloudforest (Monteverde) and am using it in a speech for visiting Costa Rica.
Size about 3,5-4 inches.

This looks like a caterpillar.

Millipedes and centipedes have chitin segments.  millipedes actually have anywhere from 40 to 400 legs. centipedes have between 15 and 177.

Looks like a caterpillar in the Saturniidae family

Probably it is Cricula silkmoth (Cricula trifenestrata, Saturniidae), in caterpillar stage.

but this is from costa rica? Cricula trifenestrata is found from India to the Philippines, Sulawesi, Java, and Sri Lanka.

Similar, but not the same. Cricula trifenestrata had white hairs coming out of the red bulbs. The picture above has black, branched hairs.


text:
Lystrosaurus was the largest creature on land in the early Triassic, why did they need burrows?
Lystrosaurus was the largest creature on land in the early Triassic, why did they need burrows? What were they hiding from?
(less seriously, why were they so ugly?)

Maybe they were hiding from the weather?  E.g. bears are pretty big, but they find places to hibernate in the winter.  Or perhaps they inherited the burrowing habit from a smaller ancestor?  As for their looks, it's in the eye of the beholder.  I think they're kinda cute :-)


text:
What is the difference between phylogroup and subclade?
Looking for clarification in terminology, examples would be greatly appreciated!
Not sure how this is off-topic. It is a general question about the difference between biological concepts defined in the field of bioinformatics.
"Questions are from students, academics and active researchers in biology and closely related fields, including:

general questions about biological concepts
questions about the biological mechanisms behind medical conditions
questions about techniques in a biological or biochemical laboratory

Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject."

The homework policy, which is linked to in the close reason, should tell you why people voted to close your question.

@canadianer this isn't homework ..... I genuinely do not understand the difference. Not taking any courses right now.

First off, I didn't vote to close. Second, some people around here have decided that "homework" includes any question that the asker does not show effort in researching themselves. This is in the homework policy as: "A question that addresses a basic biology concept that may seem trivial to biology professionals". The policy also directs you to "Research it yourself ".

PS: If you think this question was unjustly closed, you can create a post on [meta].


text:
Can we estimate effective population size from DNA sequence data (CR or cytB sequence)?
I have DNA sequence data (control region) of two population of a species. Can anybody suggest me any software to calculate effective population size? Is it possible and meaningful?

It sure is possible.
Very simple model
It is often hard to decompose the effective population size $Ne$ from the mutation rate $\mu$ though. But it is quite common to estimate $N\mu$. For example, it is a classical result from coalescent theory assuming a single panmictic population of constant size and no selection (and a few other assumptions) that
$$N\mu = \frac{S}{\sum_{i=0}^{k-1} \frac{1}{i}}$$
, where $S$ is the number of segregating sites and $k$ is the number of sampled individuals.
More advanced models
You will probably want a slightly more advance model though.
There exist a number of estimators including Colony2, CoNe, Estim, MLNe, ONeSAMP, TMVP and LDNe. I recommend having a look at Gilbert and Whitlock (2015) who compares these estimators under different demographic scenario.

Thanks, Remi. Request you to suggest some papers estimating Ne using mitochondrial DNA sequence.


text:
Which type of plants/mosses are these?
During the rainy season in India I see these miniature plants forming a light green mat over the green algae on my house's roof.

The interesting thing is they become very green and mushy after it rains. The rest of the year in dry winters and summers they go off green (kinda brown) and survive till the next rainy season.
I suspect them to be mosses/liverworts. What do you think?
Adding some more pics-

The small wood piece in the above photo is around 3 cm in length. (For comparing the size)
Temperature when these pics were taken was around 35°C and it was quite humid.

Hey guys! I did a bit of research and I think I've found it! - I think it is one of the species of Funaria


text:
Questions concerning synaptic input and dendritic processing
In the article How Spike Generation Mechanisms Determine the Neuronal
Response to Fluctuating Inputs, I read (p.11629)

I have four questions concerning some formulations:

What is "the membrane time constant" if this depends on the membrane resistance and capacitance which varies over the membrane? Maybe "local membrane time constant"? Or "mean membrane time constant"?
What do the authors probably mean with "instantaneous postsynaptic currents"? Occurring at the same time all over the dendritic tree?
What do they probably mean with "exponentially decaying synaptic currents"? The decaying of the PSPs while travelling down the dendritic tree?
What's the relation between "synaptic decay time constant" and "membrane time constant"?

(Having digested the paragraph a bit more, another - probably more accurate - reading of "instantaneous" came to my mind: "starting and ending abruptly with the abrupt opening and closing of the ion channel".)

I wouldn't suggest trying to understand this passage in terms of actual biology. This paragraph is the equivalent of the common physics trope "assume a uniform spherical cow" - they are simply describing some mathematical properties of a neuron given some assumptions. In many cases those assumptions may be very reasonable, but it doesn't make much sense to start from a uniform spherical cow and work backward into the actual shape of a cow.

I know what you mean. But the authors don't seem to be cowboys and they presumably know what they are talking about. And they obviously talk the language of actual biology (at least they use some of its vocabulary).

Started writing a comment and realized it was an answer...
These guys are basically saying "take a uniform spherical neuron" the same way you would say in physics "take a uniform spherical cow." There isn't a dendrite mentioned in the whole paper.
By "the membrane time constant" they mean exactly that: one membrane time constant, effectively the somatic time constant. They aren't talking about dendritic trees: they are essentially saying assume a uniform spherical neuron that gets inputs on its soma.
Membrane time constant is associated with the rate of change of the membrane voltage; synaptic time constant is associated with the rate of change of the synaptic current (this is what they refer to when they talk about exponentially decaying synaptic currents). Real biological synaptic currents have a time course governed my neurotransmitter concentrations and the gating properties of postsynaptic receptors. Real biological postsynaptic potentials (voltages) are governed by both the time course of the synaptic current and the capacitive properties of the membrane (i.e., the membrane time constant).
Instead of considering synaptic time constants, you could simplify a synaptic event as an instantaneous current impulse: essentially the entire current all in one instant rather than over time. The presence of the membrane time constant helps with making this assumption somewhat reasonable, because the membrane time constant ends up filtering input currents anyways, whether they are impulses or have a synaptic time constant.
In a simulated environment, you can make computations simpler by just adding a little time to the membrane time constant to roughly simulate the effect of the membrane time constant + synaptic time constant. Again, this is for computational efficiency, like when you assume a cow is spherical, not for perfect biological accuracy.

Can all of this really be true? Do these guys - who I really don't want to offend - really think of uniform spherical neurons? If so, they will have good reasons -  which in turn I would like to learn about.

I agree and I also am irritated, that they don't mention dendrites. But what does this mean/imply...?

Well they are testing a fairly specific parameter in their paper, and they want to know what effect it has on a soma-centric measure. It's much more tractable to start with simple assumptions. I'd also suggest the Magee 2000 paper that I suggested you read on another answer - as that one shows, by the time you get to the soma, synaptic properties and active dendritic processes somewhat normalize the EPSPs. If that's true, then it doesn't much matter where on the dendrites they initially came in, at least not for the integrative properties of the soma.


text:
species ID: garden bush from Bangalore, India
Please help to identify this plant. It is a garden bush growing in soil. The pictures were taken in Bangalore, India.

Please include your question where you found it, if it is wild or growing in a garden or pot, and include the photo in the question. See

The plant was found in India, near Bangalore. It is a garden growing bush.

Could be anything, if it's ornamental. However, it would appear to be some kind of Pinaceae or other evergreen conifer. Possibly a juvenile hemlock or araucaria. I know that in Northern India there is Tsuga dumosa
Maybe an Araucaria?

Those pointed, awl-shaped leaves strike me much more as a member of Cupressaceae than the other conifers mentioned (Pinaceae, Araucariaceae). If I had to guess, I'd say some kind of juniper, Juniperus, though there are many other possibilities.
Are there any other features available, like berries or cones?


text:
Would the microgravity "shape-shifting" bacteria effect have anything to do with bacteria growing in a host?
Phys.org's news article Why bacteria 'shapeshift' in space describes a recently published study Phenotypic Changes Exhibited by E. coli Cultured in Space, Zea Luis, Z. et al, 2017, Frontiers in Microbiology 8:1598, doi: 10.3389/fmicb.2017.01598.
The Phys.org article summarizes some of the results:

Because there are no gravity-driven forces in space like buoyancy and sedimentation, the only way the ISS bacteria can ingest nutrients or drugs is through natural diffusion, said Zea. The large decrease of the bacteria cell surface in space also decreases the rate of molecule-cell interaction, which may have implications for more effectively treating astronauts with bacterial infections in space.
The new study also showed the bacterial cell envelope—essentially its cell wall and outer membrane—became thicker, likely protecting the bacteria even more from the antibiotic, said Zea. The E. coli bacteria grown in space also tended to form in clumps, perhaps a defensive maneuver of sorts that may involve a shell of outer cells protecting the inner cells from antibiotics, said Zea.
In addition, some of the E. coli cells also produced outer membrane vesicles—small capsules that form outside the cell walls and act as messengers for cells to communicate with each other, Zea said. When cells with such vesicles reach a critical mass they can sync up to initiate the infection process.
"Both the increase in cell envelope thickness and in the outer membrane vesicles may be indicative of drug resistance mechanisms being activated in the spaceflight samples," said Zea. "And this experiment and others like it give us the opportunity to better understand how bacteria become resistant to antibiotics here on Earth."

I'm wondering how likely the following part of the quote from the corresponding author is to be true: "...which may have implications for more effectively treating astronauts with bacterial infections in space."
If I understand correctly, *ll of the effects related to growing in space that are described seem to be related to growing in a liquid culture medium, not inside a mammalian host. I'm not sure a bacteria which has infected an astronaut or other mammal in space will experience any difference in conditions if the host is in microgravity vs being in normal gravity. The differences seem to be specific to transport mechanisms in the culture medium, and not to any effect of weightlessness on the bacteria themselves.
Am I missing something?

Be it a host or a culture medium, the micro-environment for the bacterium is the same: "because there are no gravity-driven forces in space like buoyancy and sedimentation, the only way the ISS bacteria can ingest nutrients or drugs is through natural diffusion". Have in mind that, for the bacterium, the mammalian host is indeed a liquid culture medium.

@GerardoFurtado can you consider posting that as an answer so I can see how well others agree with it? I believe there are several transport mechanisms in living organisms that do not exist in a culture medium, from circulation of blood down to intracellular transport. A living mammal is not the same a bottle of liquid.

Thanks, but as I told you before (your question about nitric oxide), I'm avoiding writing answers here at Bio SE for complex questions like yours. If you don't write an answer with two dozen references and four sections people downvote you. As a personal rule, now I only write answers if it takes me less than 5 minutes... oh, and species-id, I like those questions: easy to answer and nobody bothers you. Anyway, I hope someone helps you here, good luck.

@GerardoFurtado very well then, this one is for you! Species identification; clusters of big plump red bugs in Taipei


text:
Species identification; clusters of big plump red bugs in Taipei
I saw these red insects in Taipei near XinBeitou MRT station in the last week of April 2017, around lunch time. They were fairly active and would keep checking each other out with their antennae for a moment and then move on to the next. What struck me was the wide range of sizes and development in the groups. I didn't notice any feeding or mating that I could recognize, just a lot of walking around and checking each other out.
There are plenty of birds around (this is quite a green area) but I didn't notice any interest by birds in eating them.
I've also included a screenshot from google maps so you can see the location and the trees growing in these concrete structures.
The body of the largest individual is probably 2.5 centimeters long.

@Charles photos of 25mm bugs taken by a ~6mm cube camera in my cellphone. I don't know how they do it!

@uhoh  我想去台湾..我能和你一起生活吗？ 哈哈

@Charles I live here but I can not read Chinese. However, I asked google and it said that my place is too small, sorry! :-)

@uhoh Oh, haha, my mistake. I suppose that's what I get for assuming! And that's a shame.. I've been trying to visit China for almost a year now. A friend of mine says Taiwan is a perfect middle ground of USA and China, so that's truly where I want to go! Best of luck to you :)

@uhoh since this is not Pyrrhocoridae I deleted my comments.

@GerardoFurtado Thanks for your help, rostrum tutelage, and for reminding me that I had a species identification question I'd been meaning to ask.

@uhoh I wish all species-ID questions were like yours here.

I'm fairly certain these true bugs belong to the species Leptocoris vicinus, and carry the nickname of "soapberry bugs", which is specific to the subfamily Serinethinae. They're quite common in urban areas of Southeast Asia, which coincides nicely with where you encountered them.
Also, you had mentioned,

There are plenty of birds around (this is quite a green area) but I didn't notice any interest by birds in eating them.

Soapberry bugs, as well as many other types of insects, are able to freely congregate in large numbers, and in such exposed places, due to their bright coloration. Having such a bright color may indicate to some predators that the prey in consideration is toxic, a phenomenon referred to as aposematism.
 source
 source
And then, here's a map of their distribution, with Taipei holding marker #37. (source)

An interactive version of this map can be found here.

wow Wow WoW WOW! A map of bugs, how cool! The bugs in the two photos certainly look like the same thing. Can you add the source of those images to the answer? Are these still nymphs? I noticed that in the photo in your first link the nymphs look just like this except for the striped pattern.

Yes, they are still nymphs. And, the sources I used for these images were chosen because they were of the best quality from what I could find, however, they aren't from distinguished sources. Instead, I chose them because they originate from people who live in Taiwan. With that in mind, in combination with the distribution of this insect, suggests the species. There does exist a Leptocoris augur, which is often confused with L. vicinus, however, the most noticeable difference between the two is coloration, with L. augur demonstrating more of an orange, as apposed to a true red.

Ya, I see now that the images are widely circulated. OK I think we can consider this one case almost closed. Thanks for your help and speedy answer!

@uhoh And as for the image you're referring to, the one that shows stripes on the abdomen of the nymph -- those are the variety of this species located in Australia.   "Thanks for your help and speedy answer! " -- You're quite welcome :)


text:
de novo assembly applications
Hey I hope this question supposed to be in this forum.
I'm not from the biology community, I'm from the data security community so im not familiar with the words you might use for answers
I need to use an algorithm that very similar to the de novo assembly algorithm.
I'll try to explain myself better I've some sequences of '1' and '0' all of them are pieces of one big sequence.
I've seen some applications that work with this algorithm such as SPAdes tadpole and Geneious but i couldn't make any of them to work for me except the Geneious because it was the simplest.
Geneious is not good for me because i need something that i can use by command line in the terminal
what application do you recommand me to use that i give input the sequences and the output will be the big sequence.
BTW, in the Geneious I've used a FASTA file for my sequence where my '0' and '1' translated to 'C' and 'D'
Thank you very much wait for your answers :))

Can you elaborate on what kind of data you're trying to assemble de novo? I've never heard of anything like this before.

You can try Velvet, but you'll likely end up with thousands of contigs unless your expected reference genome is pretty simple. This question hits many of the difficulties with de novo assembly. I'm also not sure what you mean by this:

BTW, in the Geneious I've used a FASTA file for my sequence where my '0' and '1' translated to 'C' and 'D'

Are you trying to use this for a purpose other than actual genome assembly? You say you're from the data security field, so it's unclear what's your end goal. If you only have a binary sequence, you better have a really long read length and hope there aren't too many repeats or you'll really have issues finding a consensus sequence.


text:
Are cells electrically neutral or charged to setup the membrane potential across them?
While studying about membrane potential I usually come across the Na K pump . But I can't understand does it cause any generation of net charge in the cell If yes then how do charged cells stay together with other similarly charged ones ,  if not why and how not .

It isn't neurons that are charged, it is their membranes. From the distance of other cells, they "see" both the charges inside and outside the membrane, so there isn't any substantial repulsion on that scale.
The charge across a membrane comes mostly not from the Na+/K+ pump directly, but due to differential permeability of the membrane to different ions. Ions normally tend to flow down their concentration gradients, but that flow can be influenced by an electrical potential. From the perspective of just Na+ and K+, there is more K+ inside the cell and more Na+ outside, and more permeability of the membrane to K+ than Na+. Therefore, the inside of the cell will be negatively charged at equilibrium where the net flow of ion charges is equal. At a negative resting potential, the negativity of the inside of the cell equalizes the net flow of potassium out with the net flow of sodium in. However, the actual concentration changes involved are miniscule. From the perspective of ion counts, there are basically as many positive ions inside as there are negative ions inside a cell; it's the very minute imbalance (fractions of a %) that gives a potential of ~-70mV.

Look via the Na K pump we are pumping out net positive charge however miniscule it be how does it get balanced Or does it get balanced at all.

The imbalance of charges from the Na/K pump doesn't actually matter much because ions can flow across the membrane through channels. You should just think about the Na/K pump as establishing a concentration gradient and ignore the 2 versus 3 ion imbalance. It just doesn't matter. The channels are a lot more important. The Na/K pump by itself can provide a couple mV but not the ~60-80mV that is typical.

But i still can't gauge whether cell turns out to be neutral or not


text:
Why does chromosome inversion happen?
I read that chromosome inversion is a type of genetic mutation.

Why does inversion happen? What is the purpose?

I also read that if genes do not match up during cross over between inverted chromosome and non-inverted chromosome could cause birth defect.

Then would that make chromosome inversion fall under harmful mutation?

In addition, there are two types of inversions: paracentric and pericentric. The difference between these two inversions is that one of them invovles centromere and the other one does not.

What is so important about centromere?

And lastly,

Does inversion happen before humans are born, or after they are born? When does it happen?

I apologize if my questions are vague. I do not have much background information on chromosomes.

If you are free I suggest you to red this excellent piece which answers few of your questions - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946949/

Why does inversion happen? What is its purpose?

Like many other mutations, inversion is generally a neutral mutation. Many inversions, especially those which are between small, intergenic regions, evolve neutrally by drift alone. However, selection can, and does, occur when:

inverions create structural problems with meiosis, like pericentric inversions
a breakpoint disrupts open reading frame or alters gene expression
inversion carries one or more selected alleles

Thus, inversion does not necessarily yield any advantage, but it usually does not cause any harm either (Kirkpatrick, 2010).

Can chromosome inversion fall under harmful mutation.

No mutation is useful or harmful by default. It depends on what effect it gives in every case. Similar is the case with chromosome inversion. It is mostly a nuetral mutation, occasionally harmful, and rarely useful for the individual. Thus, in a way, it can be classified as a neutral mutation.

What is so important about centromere?

The main point to ponder is how the two types of inversion affect daughter cells, especially during meiosis. For introduction, in a paracentric inversion, the centromere is not involved, while it is in pericentric inversion.
Now consider paracentric inversion during meiosis. Start with a diagram:

Due to a paracentric inversion during a crossover, formation of a dicentric bridge and an acentric fragment takes place. While the acentric fragment, due to lack of a centromere, is lost from the genome, the dicentric bridge forms such structure that the two remaining chromatins lie farthest apart. Eventually, due to tension, the homologous chromosomes break apart, leading to formation of chromosomes lacking certain genes. This makes the gamete and/or the zygote inviable, and reduces the recombination frequency.
Now, while very similar thing happens in pericentric inversion, the mechanism is a bit different. Again, see the diagram first:

Since the centromere is also involved in inversion, the genes on both arms of chromosomes are, as a result, inverted. When crossover takes place, both homologous chromosomes receive two copies of one fragment and no copies of the other. As a result, again, the gamete and/or zygote is inviable and the recombinant frequency is reduced (Griffiths et al, 2000).

When does chromosome inversion happen?

Just like all other mutations, chromosome inversion can occur at any stage of life in an individual. It is not limited to meiosis, it can occur in any replicating cell in the body. However, the phenotypic effects are most prevelant when it occurs during meiosis, since it can easily lead to defected or inviable progeny.
References:

Kirkpatrick M (2010) How and Why Chromosome Inversions Evolve. PLoS Biol 8(9): e1000501. doi:10.1371/journal.pbio.1000501
Griffiths AJF, Miller JH, Suzuki DT, et al. An Introduction to Genetic Analysis. 7th edition. New York: W. H. Freeman; 2000. Inversions. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22042/

"...selected through random drift". This is a contradiction in terms.

@gerardo I couldn't think of a better word ;) thanks though

Just remove all that part. So, instead of "inversion is generally neutral and evolves through random drift" just write "inversion is generally neutral."


text:
Reducing the Proportion of Phenotype in Hardy Weinberg Population through Selection
I was given the following question:
You travel to an unknown island and find a population of strangely colored
slugs! Upon close investigation, you notice that 16% of the slugs have a
shriveled tails, a most terrible condition you decide to name Yilunemia. The condition makes the affected slugs have a 50% chance of surviving to
reproduce. This is a autonomic recessive condition caused by a single gene,
and heterozygotes are not affected.
Assuming Yilunemia confers no discernible evolutionary advantage, how
many generations should it take for the proportion of slugs with the Yilunemia disease to fall below 5%?
Possible answers:

5
6
7
8
9

I've tried to apply usual formula for frequency after selection:
0.36 + 0.48 + 0.16 = 1
0.36 + 0.48 + 0.5 * 0.16 = 0.92
Divide by 0.92 gives:
0.39 + 0.52 + 0.087 = 1
If I keep doing this, after the 3rd generation, the frequency of Yilunemia condition is 0.045, which is less than 5%. However, this isn't an answer choice, therefore I must be doing something wrong.
Any suggestions?

The theory
You have to use the diploid selection equation (see here). Let $p$ be the the frequency of the recessive allele of interest, you get
$$p' = \frac{p^2 W_{aa} + p(1-p)W_{aA}}{\bar W}$$
, where
$$\bar W = p^2 W_{aa} + 2p(1-p)W_{aA} + (1-p)^2W_{AA}$$
You can simply iterate over with this equation. Do no forget to recompute $\bar W$ at each generation as the allele frequency changes, so does the mean fitness $\bar W$. Also, do not forget that we are looking for the generation where the frequency of sick individuals is lower than $0.05$, that is the generation where $p<\sqrt{0.05}$.
I don't think this recursion equation has any general solution unfortunately. This would mean that iteration is the only way to got.
The practice
I am a bit too lazy to compute everything by hand so here a short R code that will do the calculations for us.
frequencySickIndividuals = 0.16
p = sqrt(frequencyHomozygoteRecessiveMutants)
waa = 0.5
waA = 1
wAA = 1
for (generation in 0:10)
{
    frequencySickIndividuals = p^2
    cat(paste0("Generation ", generation, " frequency sick individuals = ", frequencySickIndividuals, "\n"))
    p = (p^2 * waa + p*(1-p)*waA) / (p^2*waa + 2*p*(1-p)*waA + (1-p)^2*wAA)
}

It outputs
Generation 0 frequency sick individuals = 0.16
Generation 1 frequency sick individuals = 0.120982986767486
Generation 2 frequency sick individuals = 0.0935350533786218
Generation 3 frequency sick individuals = 0.0738632061510922
Generation 4 frequency sick individuals = 0.0594638505565122
Generation 5 frequency sick individuals = 0.0487003101360286
Generation 6 frequency sick individuals = 0.0404940467744661
Generation 7 frequency sick individuals = 0.034123112395776
Generation 8 frequency sick individuals = 0.0290951856295452
Generation 9 frequency sick individuals = 0.0250680151553009
Generation 10 frequency sick individuals = 0.0217991643532054

So, it actually takes 5 generations to reach an allele frequency lower than $\sqrt{0.05}$.
Source of information on hardy-Weinberg problems
Note by the way, you might be interested in having a look at a tutorial on how to solve Hardy-Weinberg problems on the post Solving Hardy Weinberg problems.

I understand how to do it this way. I was thinking, given that I have no shouldn't take more than 1.5 minutes or so to (according to problem guidelines), if this is the fastest way to solving the problem.

Please see edit.


text:
Why isn't the sticky bud plant more widespread
Why isn't the sticky bud plant (Galium aparine) everywhere around the world? Because to me it seems that it has the best method of seed dispersion/transportation (wiki link: https://en.wikipedia.org/wiki/Galium_aparine)

Can you link up something on the "sticky bud" plant?  I would like to read more about it.  I suspect there may be more than one plant with sticky buds.

Cleavers are distributed all over the world. The link you provide answers the question. (They shouldn't be able to grow in the desert.)

As already pointed out in comments, Galium aparine is actually very widespread, according to wikipedia it occurs in "a wide region of Europe, North Africa and Asia from Britain and the Canary Islands to Japan. It is now naturalized throughout most of the United States, Canada, Mexico, Central America, South America, Australia, New Zealand, some oceanic islands and scattered locations in Africa."
Because it occurs on moist and rich soils, it doesn't occur everywhere. It is unable to grow on dry and nutrient-poor soils (like deserts and steppes). But it is also absent in frequently mown grassland.


text:
How can just random mutations explain mimicry?
I have been reading this article on drug resistance which explained that how random mutations in a bacterial colony can lead to development of drug resistance among some organisms in that colony.
A thought occurred to me that if mutations are just random (by random what I know (or think)  here is the number and time of a mutation occurring in an organism in a normal environment may not be fixed but random) events arising from copy errors during DNA replications then how come some animals in nature mimic their surroundings to save themselves from predators or catch prey?
Let's consider for the time being that an animal exhibiting mimicry have evolved through natural selection, after suffering a mutation in their DNA which made them well adapted to their environment, and also saved them from their predators. Now we know a fit organism, in the struggle for existence, produces offsprings which can withstand the adversities of the surroundings and thus increases in numbers. In this way we may assume that due to many such helpful mutations led to the evolution of a new species.
This may sound simple but it actually seems to me as an over simplification of the events that lead to the development of 'that' new species. First of all not all mutations are helpful. Some are lethal as well. Also mutations may often be silent due to the degeneracy of the genetic code and presence of introns in the eukaryote. But let us consider here that the mutation suffered by our test organism was neither silent nor harmful, that too leaves us with infinite number of mutation possibilities to get a favourable organism from an unfit (to the surrounding in which our test organism is struggling) parent generation. Thus I think nature may not test each and every kind of possibility to select the fit one because in that case the test organisms will be far too many in number. Also if we consider that the fit one emerged just by chance out of million other possibilities then its sure that it was either too lucky or there is some other factor except 'just' mutation which can explain mimicry. Thus can only general mutation explain mimicry or we need something more to explain it?

poss. duplicate: https://biology.stackexchange.com/q/66183/5198

Possible duplicate of Are mutations random?

@BryanKrause actually Remi b. added the question after I  asked this one, he added it as according to him many people get confused about the matter. Moreover I have actually asked 'if mutations are random then how can we  explain mimicry shown by organisms'.

@jyotiproy Duplicates don't have to be later than the original to be closed, and closing as duplicate is not meant to say "this is a bad question", it just means "this question is answered somewhere else." It would make more sense to point to that new Q&A rather than have this one be the example forever, because that one is more general and covers a common question here.

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.

can anyone please help me to shorten this question. It has been occurring to me for weeks and I am desperate for an answer. I have asked this to my teachers too but failed to get a satisfactory answer.

@jyotiproy your issue is your question wanders all over and makes it really unclear why you think NS cannot explain mimicry, this makes the question unanswerable without explaining everything about evolution in detail which would be way too broad. Consider looking into the difference between selection which is random (enough) and selection which is the opposite of random.

@John I wanted to know that whether NS explains mimicry? If so then how can the random mutations be so perfect that it mimics another unrelated organism completely? Is it by chance or there is a controlling factor behind it?

/how come these animals (below) show such striking resemblance with their surroundings/
You are looking at the culmination of millions of generations of these insects.  The mutations are random, but only the helpful ones (of all the random ones) produce an advantage for the organism and so persist in the species.   If a random mutation caused an insect to look slightly more like its environment, that insect might do better at avoid predators or catching prey.   Thus it would be more likely to produce offspring which would also have its mutation.  Random mutations that caused an organism to look some other way would not confer any benefit as regards producing more offspring.
In each generation, if there is some random mutation that made the organism more similar to its environment, it could produce better fitness.  The end result, over thousands (even millions) of years, is an organism which looks very much like its environment.
Fitness is what drives evolution.  Read more at the link if you are interested.  The more offspring I have the more I pass along my DNA and the better my fitness is.  If I have a mutation that lets me have more offspring, that improves my genetic fitness.

In each generation, if there is some random mutation that made the organism more similar to its environment is wrong. Fitness is what drives evolution.  and The more offspring I have the more I pass along my DNA and the better my fitness is are misleading. Also, the overall phrasing is quite unusual

@Remi.b - do you mean by this that random mutations (which change the appearance of an organism) cannot increase fitness?

No, this is not what I meant. First sentence I quote, I mean that mutation are not directed toward increasing individuals fitness (it is the opposite). Second sentence I quote, I mean that there is much more to evolution than juste natural selection and third sentence I quote I mean that there is a reversal of the cause-consequence logic. I would add that the term random mutations does not mean much (see Are mutations random?)

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.

Are mutations random?
I decided to open a new post (and directly attempt at answering it) as this claim is very common and a bit misleading. See Are mutations random?.
Your question does not need to be specific to species looking like their environment
You seem to not understand the basics of evolutionary biology. Your question is specific to why organisms look like their environment but what you should simply understand is the basics of evolution and selection.
You should definitely have a look at an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for more information.
How can there be such striking similarities between some organisms and their environment?
Natural selection is the (main) answer.
An important reason (but definitely not the only one) for why a population of organisms would evolve to look like their surroundings is camouflage. Camouflaged organisms can typically have a higher fitness in a population that suffers from visual predators.

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.


text:
response elements in transcription regulation
I'm studying eukaryotic gene regulation and I want to know whether there are some instances where transcription factors don't need to bind to response elements to initiate transcription. RNA polymerase can directly bind to the DNA.
I can't find any evidence for this. Does anyone know of a case that exhibits this?


text:
Negative RNA virus
I have tried to see how this works but I can't find any helpful information. How can a negative strand RNA virus make protein during an infection?

Then you did not search enough. It took me 2 google searches to find that the virus uses RNA dependent RNA polymerase to convert -ve sense RNA to +ve sense mRNA. Also the virus particle itself contains the polymerase. Link - https://microbiologybytes.wordpress.com/2008/02/04/negative-sense-rna-viruses/


text:
Can anyone tell me what type of worm this is?

I sure hope you can see this picture. Need to know what type of worm this is. Found one in July and one just now inching its way across my tiled floor. I live in Florida. It is one color all the way around, dark red.

I can't see the head clearly but based on
1: it is a big worm cruising around on land
and
2: you have never seen one before
I bet on this

From linked article.

The flatworm (Platydemus manokwari) has few natural predators outside
  of New Guinea, and it likely will have no predators in the United
  States, Justine says. It gobbles up soil-dwelling invertebrates like
  snails, which could have a big impact on the environment.

I checked wiki for this worm and it says it has a lighter colored underside. This worm is the same color all-around

Does your worm have a semicircular head?  Or a pointy head like an earthworm?

I'm not sure. I don't know anything about worms but I think it has a pointy head?


text:
Why do humans seem to be the only mammals that like spicy food?
Peppers evolved chemicals like capsaicin to discourage animals from eating them, and that chemical itself can cause internal damage if consumed in large quantities, though this is usually only a concern for the hottest of peppers (which people do eat).
Still, why is it that humans seem to be the only animal that often "like" spicy food?

Since I can't quote any literature on this I wont write it as an answer. My guess would be that other animals don't have the ability to feel the "rush" we get from punishing ourselves by eating spicy food. For example the burning sensation from chilly releases endorphins which gives you a temporary biological "high". I am also eagerly waiting for an expert to answer this.

"Peppers evolved chemicals like capsaicin to discourage animals from eating them"... that is not correct. It's to discourage mammals from eating them. Birds eat chili without any problem.

But the observation remains the same. Humans are mammals and often like spicy food, and there are other animals comparable to humans in many ways which do not like spicy food by their seeming intrinsic physiology. The question still remains: why is it that humans to are an exception from this group? Perhaps its something similar to broccoli where some people taste it as especially bitter and others do not, but you have not provided any formally recognizable answer.

@DaneJoe Not all humans enjoy spicy food. In fact, many don't. And of those that do, there are even fewer who enjoy really spicy food. Your question could very well be asked when only considering humans, which could suggest then that there's nothing inherent to [all] humans having an affinity towards spicy food. This, however, is the basis for your question. BTW, my cousin has a cat that eats spicy food all the time. Also, I believe birds eat all kinds of [spicy] peppers..

The same question could be asked about acid or bitter food. I would think the answer lies in our cognitive abilities. Somehow, we just happen to have built a culture for liking those types of food we've been selected for not liking.

Perhaps the answer is that humans seem to be the only species that is capable of seasoning its food.  Very few people eat hot peppers directly (and then it seems to be more of a test of machismo that actual liking, at least IMHO), they use small amounts to season food.  Certainly my dogs have eaten such food with every outward evidence of liking.

Only TWO known mammals like spicy food. source

There are really two questions here  1. Why do humans use spices? and 2. Why do some humans eat excessive amounts of this particular capsaicin but not other spices, or only a few others?
I will answer the second question first. The current understanding of why some humans eat so much spicy food is that it is a form of benign masochism. "Some" is the key: only some humans like spicy food in anything but the most minimal amounts. It has been shown that eating spicy food releases endorphins, but only after the burn, so eating spicy food is like going to a scary movie or riding a rollercoaster — initial discomfort followed by a rush. Humans are the only animals that do these things because we know they are not dangerous. It is thrill-seeking.
Now this is not the entire story. Spices in general have their own origins.  Many spices inhibit bacteria, and capsaicin appears to do so as well. This alone could be the reason people started using it more widely. We see that more spices are used in warmer climates, the same places where spoilage would be the biggest risk.  We also see more use of the spices with the highest inhibitory properties. Interestingly humans may not be the only animals to spice food in this way; bears and bees are both known to mix antibacterial plants into stored food.
Additionally small amounts of many spices, even capsaicin, can improve flavor  without generating the burn. This is probably the least understood aspect, but some believe it may be linked to simulating the flavor of better-quality organ meats or increasing bioavailability of some nutrients.
Lastly it has been shown that capsaicin in particular can actually trick the body into cooling itself off even when it would not do so normally. Your body responds to the false signal of heat by cooling itself, which could be a benefit in hotter climates.

Yes, I was going to answer with "benign masochism" also.. The examples of "from negative to positive" experiences are called hedonic reversal.

Here is a relevant article and a relevant excerpt about animals: "There is no
strong evidence for liking for innately negative experiences
in animals. The strongest evidence against animal
exemplars is that rural Mexican dogs and pigs that eat
food with hot peppers regularly (since they eat human
leftovers) do not develop a preference, unlike some hundred
million human Mexicans who share their diet (Rozin
& Kennel, 1983)"

Birds for instance can "ingest" spicy food, but that doesn't mean they actually perceive the spiciness in the same way or at all. If someone can't taste the acidity sulfuric acid, they could drink sulfuric acid and say they liked it.

@DaneJoe it isn't spicy to birds, capsaicin only works on mammals.  birds don't have the same TRPV receptors as mammals, which works for the plants because birds spread the pepper seeds, mammals destroy the seeds when they eat them (chewing) so the pepper want to discourage mammals but not discourage birds.

Right, so when people try to argue that birds have no problem with spicy food, the point is moot.

@DaneJoe correct, chili peppers are not spicy to birds, the closest things to spicy you have for birds is things like mustard, wasabi, or black pepper.

I think like many things spicy food became something that we used as a tool. Used mostly for preserving food, those countries where it gets very hot due to a tropical climate you'll find the food tends to be much spicer in areas where parasitic flies and other pathogens would contaminate the food faster. The spicier it is, the longer your food stocks would last. Over generations they developed a higher and higher tolerance.

Welcome to Biology SE! It'd be great if you can cite your sources. Answers with no references may be challenged or deleted.