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How evolutionarily conserved are UTRs?
Coding sequences of genes have a certain degree of evolutionary conservation, so that comparisons based on sequences (BLAST, HMMER etc) can be informative. Generally speaking, the more two species are phylogenetically close to each other, the more their genes will be similar to each other. To add to that, different genes will have different degrees of sequence conservation - for instance, histons are very conserved and so on.
Do these considerations hold true for untranslated regions of genes (both 5' and 3')? To what extent can an alignment of UTRs be meaningful? Are there any very conserved UTRs as there are very conserved CDS? I know that there are some conserved motifs in 5' and 3'UTRs, but what about the overall sequence?

Depends on the gene but, in general, less than CDS

Can you please clarify what you meant by "for instance, introns are very conserved"?  Did you mean exons?  Introns are generally less well conserved than exons.  Also, introns are parts of genes not genes so this doesn't seem to be a relevant example to give.

@tyersome Oh sorry, I meant "histons", not "introns". I just wanted to make an example of a very conserved gene.

I assume you mean histones not histons. In which case why don't you download sequences of human and mouse histone mRNAs from Genbank and compare them by one of the many online programs available to do so? The overall conservation is likely to be low (it is for actins), but this does not preclude more subtle conserved features.

@David ...yes, sorry, English is not my first language so I get confused. I'm not interested in levels of conservation in histone sequences, I'd like to know how conserved are UTRs at a broader phylogenetical level. I found this article (https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-018-4821-8#Sec10) about 3'UTRs in cichlids and non-cichlids, but not much more.

This is a question specific to the organism, assembly, and genes of interest to you. You can answer this yourself with a bit of elbow grease.
You could measure mean phyloP or phastCons conservation signal over UTR-annotated intervals, and compare it against the background mean conservation signal over random, mappable regions of the genome of similar length (i.e., calculate the mean and variance in UTR length and sample mappable regions of the genome for intervals with the same distribution).
At a very basic level, you could perhaps apply either the U-test or Wilcoxin rank-sum test, depending on your assumptions of dependence, whether your background does or does not include UTRs.
One source of phyloP and phastCons signals for various genomes and multi-genome alignments is UCSC Goldenpath. For example, here are phyloP 100-way alignments to hg38. You might get UTR annotations from Gencode, assuming you are working with human or mouse. To do interval overlaps and mapping/statistics operations, you might use gff2bed, bedops, and bedmap in the BEDOPS toolkit(*), and then use R to do statistical tests.
Disclaimer: I am one of the authors of the BEDOPS toolkit.


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What flower is this? (Dolomites, Italy)
I took this picture a few days ago in Val Rendena, in the dolomitic Brenta group (2000 m). The whole plant was 15 cm tall at most, and it had a single leaf on the stem. What flower is it?

How was the leaf ? (Shape, texture...)

I had a look at white-flowered plants flowering in July in a site about the flora of the French Alps, and the best I could find was Parnassia palustris:
http://www.florealpes.com/fiche_parnassie.php

At this developmental stage, it looks quite similar to your photo, with the same kind of structures at the base of the petals.
The site says that there are heart-shaped leaves at the base, plus one on the stem. This last leaf matches your description. The site says it can grow up to 2500m.
The Italian Wikipedia says:

In Italia è presente solo nelle regioni settentrionali e centrali, nonché in Campania.[2] In montagna si spinge fino a circa 2000 m, ma sulle Alpi è stata segnalata anche a quote superiori (3000 m sul versante svizzero del Monte Rosa).

This means that it can be found in the Italian Alps too, including at 2000m.

source: Stack Exchange

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How does acacia affect the growth of nearby plants?
I know acacia will make the soil more acidic, but how? I tried to search online, but cannot really find something useful.

What is the source of the claim that acacia makes the soil more acidic?

@LinuxBlanket My teacher told me that it will

The only hint to acacia making soil more acidic I could find at all was this: http://crcleme.org.au/Pubs/Advancesinregolith/Leonard_Field.pdf There it is somewhat stated that because they fix nitrogen, the soil acidity increases around the root. I don't know what to make of this at all, I was just curious and found it unexpectedly hard to find information on.

You say "affect the growth of nearby plants". Is this interaction positive or negative for the other plants?

try reading articles similar to here and here and update your post with what you've learned. We expect question askers to do their own research before posting questions. See the help page for asking good questions. Thanks.

According to Wikipedia:

Allelopathy is a biological phenomenon by which an organism produces one or more biochemicals that influence the germination, growth, survival, and reproduction of other organisms. These biochemicals are known as allelochemicals and can have beneficial (positive allelopathy) or detrimental (negative allelopathy) effects on the target organisms and the community.

Now to the Acacia case.
First of all, Acacia is a genus comprehending almost 400 species, so my answer will cover all allelopathy cases involving one species belinging to this genus.
This article states that Acacia mangium leaf extracts and forest soil negatively affects germination and growth of paddy, and this other one reports phytotoxic effects of Acacia melanoxylon on Lectuca sativa (lettuce) germination and growth.
As to how Acacia species can have an allelopathic effect on nearby plants, this article evaluated the content the phytochemical composition of Acacia cyclops, Acacia mollissima and Acacia cyanophylla pods and seeds and the phytotoxic effect on lettuce seed sprouting. It states that:

All extracts of the three species of Acacia contain saponins and condensed tannins.
The most toxic one was the ethyl acetate extract of seeds from A. cyanophylla, a total inhibition of growth (100%) was registered.
A new triterpenoid saponin called mollisside B has been registered for the first time in the Acacia genus and may be responsible of part of the allelopathic effect on lettuce.

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Octopus behaviour

When visiting a museum in Malmo my friends and I came across this little guy. While we observed him wandering around his tank he suddenly opened a channel on the side of his head and shot some red string out of it. The string seemed kind of sticky, nothing like ink. We are still wondering what it was and why he was doing it. Maybe some kind of defensive behaviour or just usual octopus stuff?

Just a guess, but could the octopus have been pooping?
This is a gif of an octopus pooping. It matches your description except for the colour, so I'm not quite sure. Did it look like this? Also, could the substance look red because of the tank lights? After all, your photo looks weirdly violet overall.
Fun fact: octopuses have their anus channeled in the siphon (the "channel on the side of his head" you observed) and this has been object of a question here in Bio.SE.

Was also one of our guesses. The link doesn’t show a pooping octopus though. Really just that foto, we had plain sight on it.

@PeterS whoops, sorry, now the link should redirect you to the correct page...

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Please give information about this insects

I took this photo of a small insect which I found near to my house (Maharashtra state, India). What insect is this?

Welcome to Biology.SE! Take the tour to learn about this site and earn your first badge. Also, you have to tell us where and when this photo was taken in order to increase the chances of identifying this insect.

It is definitely a member of Membracidae. A treehopper. Order Hemiptera.

It looks like an insect belonging to the family Cicadidae. Further information is needed to identify this cicada species.

@SachinPrabhu I'm not sure about my answer, where did you find the insect exactly?

In India state Maharashtra where

This isn't a Cicada: it's a treehopper (family Membracidae) but not knowing the Indian fauna of the family I can't go any deeper.

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How much time does it take for an evolutionary change to take place?
I think I've read that in humans, it takes either 50,000 or 100,000 years for a mutation to fixate. But I've looked into the books I thought it mentioned it and I can't find it. I know there are theories that behavioral modernity has arisen before 40,000 years ago, and that modern humans evolved from Homo heidelbergensis, Homo rhodesiensis or Homo antecessor, some 100,000 to 50,000 years ago,  but I don't know if this implies the same. Anatomically moderm human . On the other hand, this other article (7 years old now)  says evolutionary change might take 1 million years (Not so fast).
How much time takes for an evolutionary change to take place in animals in general, but also in humans in particular? (if there is any difference between humans and the rest of the animals. I know mutations don't take the same time to spread in animals than in bacterias, for example)

I think the term you're looking for is "fixation". The fixation of a mutation is its presence in a population with frequency =1, that is every individual of that population has that mutation.

Are you arguing that it took 50,000 years for humans to cause the extinction of the Carolina parakeet?  Or that it takes 50,000 years for XDR tuberculosis to become common?

Any change in allele frequency is considered an "evolutionary change". So, you don't need anything to fix to get an evolutionary change.

But it seems not everybody uses it in that way, my question goes in the sense it is used in this link regardless of semantics.  https://phys.org/news/2011-08-fast-evolutionary-million-years.html . BTW, I've also seen it used that way it's used in the link, in a book

@Pablo well this popular article is awfully phrased! I can't really judge the content otherwise as the popular article fails to link to the original research paper from which they supposedly report the results.

Rather than time, you might want to measure in generations.  A human generation would be 15 years or more, rats may have 4 generations in a year, bacteria coupld perhaps manage 15 minutes or less...

Humans are known to have experienced a pretty significant bottleneck around  70,000 years ago, this alone will drastically increase the rate of fixation across that event. to the point of a single generation.

How much time does it typically take for a new mutation to fix in an animal population?
The answer can really take any number. It will all depend upon the size of the population and the selection coefficient on the mutation. If we assume neutral mutations, then we can use Kimura and Ohta (1968)'s result. They showed that the expected time for a neutral allele to reach fixation (given that it will reach fixation) is
$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$
where $p_0$ is the initial frequency and $N$ is the population size. Replacing $p_0$ by $\frac{1}{2N}$ and you get
$$\bar t\left(\frac{1}{2N}\right)=-4N\left(\frac{1-\frac{1}{2N}}{\frac{1}{2N}}\right)\ln\left(1-\frac{1}{2N}\right)$$
which can be simplified
$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(\frac{2N-1}{2N}\right)$$
Stick in any $N$ you want and you'll get your answer. Of course, this equations assume panmixie. In absence of panmixia, then it all depends upon the interconnectedness of the different populations. If some population are perfectly isolated, then a mutation will never fix in the entire species.
How much time does it typically take for a new mutation to happen and fix in an animal population?
The time to wait for the mutation to fix is typically quite negligible comparing to the time it takes for this mutation to happen. Let $\mu$ be the mutation rate. The number of mutations happening each generation is $2 N \mu$ and assuming they are neutral a fraction $\frac{1}{2N}$ of them will fix. Hence, the expected waiting time is $\frac{1}{2 N \mu \frac{1}{2N}} = \frac{1}{\mu}$. In humans, the average $\mu$ is of the order of $10^{-8}$ per site but there is a lot of variation among sequences.
So, if your mutational target is only a single site, then the expected time to fixation of a currently non-existing mutation is $10^8$ generations! If you are considering the entire genome as you mutational target is the entire genome, your mutation rate is of the order of $10$ and the expected number of generations is only $\frac{1}{10}$.

Perhaps just to add a source, the standard mutation rate in humans is approximately 0.5×10^−9 per basepair per year, and mitochondrial dna mutates quite a bit faster - so it depends what aspect of a human is being referenced. link  Cheers

@Aaron43 See edit


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Please help to identify this shrub

Please help to identify this shrub in Hong Kong:
- dark green fruit with white spot
- fruits cluster at top of stem
- upright growing of green leaves
The shrub was from Hong Kong MacLehose Country Park Trail in Tuen Mun (somewhere near a reservoir), route 10. The place was of an altitude about 200m (600 feet from sea level) hot and humid. Hong Kong weather is South of the tropic of Cancer which is equal to Hawaii in latitude.

It would help if you tell us where it grows, and whether it's wild or cultivated.  Some indication of scale would help, too.

The shrub was from Hong Kong MacLehose Country Park Trail in Tuen Mun (somewhere near a reservoir), route 10.  The place was of an altitude about 200m (600 feet from sea level) hot and humid. Hong Kong weather is South of the tropic of Cancer which is equal to Hawaii in latitude.

The plant was confirmed as Mussaenda pubescens. Common in Hong Kong but most people recognized the plant by its yellow flower and white leaf (fruit was mostly not seen concurrently).
My friend used a reversed image search smartphone app to get the suggested plant name in 30 seconds.
Mussaenda is a genus of flowering plants in the Rubiaceae family. They are native to the African and Asian tropics and subtropics.
( Mussaenda philippica in Singapore. Mussaenda pubescens in China. Mussaenda erythrophylla in China etc.)

Sources of reference are such as from:
Hong Kong - http://www.hkwildlife.net/Forum/viewthread.php?action=printable&tid=5497
Taiwan - https://bruce0342.blogspot.com/2014/08/blog-post.html

@RudyLaw You should post what was confirmed as an answer to this question, instead of a comment.


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Why can't cats run longer distances like dogs?
Cats can run about nearly 30mph. Their stamina, though, is for short distances. Why can't they run longer?
Can cats be trained to run longer distances like dogs? For instance, could their resistance improve by stair case training (running many times up and down the stairs)?

Amounts of fast twitch vs slow twitch muscles could be factor, cats are specialized as ambush predators so should have a lot of fast twitch.

Cats, both domestic and wild are, for the most part, ambush predators that catch their prey with bursts of speed. Lions and cheetahs do run down their prey, but not over long distances. Wolves chase their prey over long distances, sometimes for hours. This is a classic case of trade-offs. Humans have modified the behavior of domestic cats and dogs, but both still rely on the characteristics of their ancestors. You can build cat muscles with exercise, but you can't make them "dogs".

Canine elbow changed from allowing paws to swivel — which is important for grabbing and tackling prey — to keeping the paw more stable, which is important for long-distance running.
Meanwhile, cats maintained their tried-and-true method of ambushing prey, using quick bursts of sprinting to tackle startled beasts.(ref)
Cats and dogs diverged about 60 million years ago, and endurance adaptations for dogs started at least 40 Ma from mongoose like ancestors.
The forelimbs of African wild dogs show a combination of adaptations to endurance running, including a vestigial first digit and reorganized wrist muscles, passive spring action from a powerful ligament, and bigger muscles that store energy and provide stability. (ref)
You can see for yourself if you examine a dog's wrist and paw and check it's springiness, length, agility, grabbing ability... it's straight and springy for running.
Another know fact is that:
canines maintain a high mitochondrial protein turnover facilitating rapid adaptation to environmental extremes and energetic challenges (Miller et al, 2017, PLOS ONE 12:e0174874).
The cat's nasal channels are also less adapted to humidifying warm/cold air and tracking down prey for exhaustive predation.
Cats are typically forest animals and can climb trees better and specialize in fast attacks, including razor sharp claws where the chitin flakes a bit like flint.
You can see the cat's running adaptations when you consider it's jumping ability, climbing ability, reaction speed, attack poise, claw vs bite ferocity, limb agility, speed of movement, night vision.
They comprise a spectrum of ecological specialties that place them at different ends of the performance chart for much of their anatomy and biochemistry.

Given the diversity of cats and dogs, it is hard to generalize about the distances that cats and dogs can cover.
This question would be hard to answer even for dogs and cats of similar size, as there would be many confounding effects, such as the size of the legs, the size of the lungs, the basic metabolic rate and the motivation.
Training your cat could indeed allow it to run longer distances as its muscles develop and its amount of erythrocytes increases, but I wouldn't recommend pushing an animal too hard as it could result in exhaustion or death.

So train on the stairs could help then. I tried it out with treats my cat did 10x on 14steps that’s about 140steps he ran then he gotten tired so if he can run 2x as munch in month his stamina will grown higher and build muccel

Cats don't run long distances because their body temperatures rise quickly. This is because a cat's sweat glands are limited to a few parts of it's body, mostly it's paws.
Other mammals, such as dogs and humans have sweat glands all over their body and can therefore regulate internal body temperature for longer periods of time.

The part about dogs is untrue - they are similar to cats in this case, with the sweat glands being on the paws. They pant to keep cool...


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What kind of factors determine how someone looks according to their race or ethnicity?
From what I read, race is considered the biology, the physical traits inherited by ancestry. Ethnicity and nationality have to do with social construct and cultural identity. This is almost the same things as sex and gender, where the former means the biological characteristics, and the latter refers to the social identity.
So, is there any relationship between race, ethnicity, and nationality? For example, Asians have a different cuisine than Europeans, which consists of whole grain and wheat, which explains why they are generally shorter? What makes them have slanted eyes? Is it because they have been known to look up at the sun constantly that they developed that characteristic over time?
What makes Mexicans have black hair, brown eyes, and medium skin, or have higher foreheads? Again, does this have to do with the cuisine that they have, or something else?
The only explanation I have heard about race is that melanin affects the colour of the skin. It is always sunny in Africa, which is why Africans have really dark skin, despite the fact that all of humanity derived from Africa. Europeans lived in more cloudy weather, so their skin became paler. I'm sure there's more to these findings.

Concept of race
The concept of race often poorly represent the genetic structure of populations. There is therefore an important socio-cultural aspect to the concept of race. The first sentences from wikipedia > race make this point clear

Race is a concept used in the categorization of humans into groups, called races or racial groups, based on combinations of shared physical traits, ancestry, genetics, and social or cultural traits. Although such groupings lack a firm basis in modern biology, they continue to have a strong influence over contemporary social relations.

What explain why people of different race look different?
You should most definitely have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?
Your question can therefore be rephrased as "What is the heritability of the phenotypic trait X in humans?", where trait X could be anything of interest such as hair colour for example.
The answer for such question is always the same. It goes in three points

It depends upon which phenotypic trait you are looking at
For whichever trait you consider, it will most certainly be a combination of both genetic and environmental factor.
The evolutionary reasons for the existence of such distinction among groups will again depend upon which trait you're looking at.

If there is one particular trait that is of interest to you, you might want to open a new post to ask what is the heritability of this trait and whether there is any selective reasons for why different ethnic group differ for this trait.

You might be interested in a short and easy intro course to evolutionary biology such as Evo101 by UC Berkeley


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I found this in my refrigerator water filter. Is it a biofilm? Is it a sign of dangerous bacteria?

When I dispense water form my refrigerator after changing my filter, the following slimy tube like deposits appeared. Does anybody know what this is? Could it be a biofilm growing in the water hose, and if so, is this type of bacteria likely dangerous or benign?

The most dangerous bacteria are those that release toxins, and those that can reproduce very happily at 37 degrees inside the human body. lower temperature bacteria are not typically the most competitive at 37 degrees. you;d need to search reagents that identify biological molecules, lipids, proteins, carbs, amd run some test to identify it..  Biofilms develop with a good supply of micronutrients and nitrogen.


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Genes & Map Units
Two genes of a flower, one controlling blue (B) versus white (b) petals and the other controlling round (R) versus oval (r) stamens, are linked and are 10 map units apart. You cross a homozygous blue oval plant with a homozygous white round plant. The resulting F1 progeny are crossed with homozygous white oval plants, and 1,000 offspring plants are obtained. How many plants of each of the four phenotypes do you expect?
The answer is: 450 each of blue oval and white round (parentals) and
50 each of blue round and white oval (recombinants).
Here's how I solve it: BBrr (homozygous blue oval) X bbRR (homozygous white round) gives four times BbRr (heterozygous blue round). Then BbRr (the resulting F1 progeny) X bbrr (homozygous white oval) gives BbRr, bbRr, Bbrr, and bbrr. I don't get how the numbers 450 and 50 are related to the 10 map units apartness, but BbRr (blue round) and bbrr (white oval) are parentals.
Source: Campbell Biology 2017, page 313.

According to my book, a map unit is a unit of measurement of the distance between genes. One map unit is equivalent to a 1% recombination frequency.

What is the definition of map unit according to your book?

@LinuxBlanket, I'm Viktor but I have to have at least 50 reputation to add a comment.

Related: Genetic linkage greater than 50 centimorgans

I don't get how the numbers 450 and 50 are related to the 10 map
  units apartness,

Understanding how to use the map unit information is the point of the question.
If the B and R genes were unlinked, a gamete with the B allele would have a 50% change of having the R allele, and a 50% chance of having the r allele.  It would just be luck which chromosome went in to the gamete with the B-containing chromosome.
But in this question, the B and R genes are on the same chromosome.  Given the breeding scheme, the F1s have one Br chromosome, and one bR chromosome.  Unless crossing over happens, the gamete that gets B has to get r as well.  Crossing over happens 10% of the time.  So instead of the gametes BR, Br, bR, br all being equally likely coming from the F1, their odds are actually 5%, 45%, 45%, 5%.

The two chromosome copies that bear the alleles in the F1 are
B-{10 map units}-r  -  Blue oval
b-{10 map units}-R  -  White round

As you said, one map unit is equivalent to a 1% recombination frequency. Ten map units = 10% recombination frequency. It means that the progeny will have a blue round/white oval phenotipe only 10% of the times, while 90% of the time it'll show the parental phenotype.
Hence the 450/50 (90%/10%) proportions of the F2.


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Breathing with Clogged Nose during Sleep
This just happened to me recently, I was trying to sleep with clogged nose, so I tried breathing through my mouth. As you can imagine it was hard, but I managed to sleep deeply.
So I became curious, how does our body know whether to breathe through the nose or the mouth especially when we have a clogged nose during the time when we are in deep sleep?
NOTE: I tried researching this, but most result just shows how to clear clogged nose before sleeping

Comments are not for extended discussion; this conversation has been moved to chat.

Most people with colds/allergies/stuffy noses don't die in the middle of the night. Why?
Prevention of oxygen deprivation is powerfully regulated. If insufficient air intake is possible through the nose, the mouth opens automatically (regulated by the autonomic nervous system. If you exercise, at some point, nasal breathing isn't enough, and you start mouth breathing. It's not conscious.

The autonomic nervous system (ANS)... is a division of the peripheral nervous system that supplies smooth muscle and glands, and thus influences the function of internal organs. The autonomic nervous system is a control system that acts largely unconsciously and regulates bodily functions such as the heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. This system is the primary mechanism in control of the fight-or-flight response.
Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting. Those are then subdivided into other areas and are also linked to ANS subsystems and nervous systems external to the brain. The hypothalamus, just above the brain stem, acts as an integrator for autonomic functions, receiving ANS regulatory input from the limbic system to do so. (emphasis mine)

The answer is a complex interaction between blood pH and oxygen/CO2 receptors and the autonomic nevous system.

As a point of emphasis that I think is lost to novices of biology, the brain (and the rest of the nervous system) does a lot that you are not aware of - it seems that people often have some intuition about their "subconscious" and they think of all this high-order pseudo-Freudian stuff, but the nervous system is so good at just handling the day-to-day 'boring' nitty-gritty operation of the body that people take it for granted and it just seems magical... Respiration, circulation, digestion, all hardly noticed unless something is quite wrong.


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How does the counter-current multiplier work in the nephrons?
Why is the counter-current multiplier called like that? What is flowing in the opposite direction to the glomerular filtrate for it to be called "counter-current"?
Can you please explain the counter-current multiplier mechanism in the loop of Henle in the nephron, including details about the ascending limb, descending limb and the collecting duct?
I have searched it everywhere and I cannot find a satisfactory explanation that I can fully understand.

Countercurrent multiplication

What is flowing in the opposite direction to the glomerular filtrate for it to be called "counter-current"?

The filtrate is moving in the opposite direction of the filtrate. It's a loop. Filtrate moves in two directions relative to the nephron, down (from the cortex toward the papilla/through the medulla) and up (from the medulla to the cortex). We'll start with up, because that's where the active transport occurs

Up: as filtrate moves up the ascending limb, $Na^+$, $K^+$ and $Cl^-$ are actively pumped out of the filtrate and into the surrounding ECF. This limb, the ascending limb, is impermeable to water, so water doesn't follow the active transport of solutes and the fluid becomes more concentrated in the ECF than in the tubule lumen. So on the way up, the filtrate becomes more dilute.

Down: the descending limb is permeable to water and to ions along with it, so as filtrate moves down the descending limb, the osmolarity of the filtrate equilibrates with the concentrated ECF. This equilibration between descending limb filtrate and the ECF, makes the filtrate more concentrated, so on the way down, the filtrate becomes more concentrated.

By itself, the active transport of solutes out of the filtrate and into the ECF on the way up the ascending limb, (with dilution again by the water on the way down the descending limb) would seem to make only a small difference, but consider what happens as the filtrate continues to flow, while the ECF doesn't.
Consider this diagram from Constanzo Physiology, Chapter 6:

First, the active transport of solutes out of the ascending limb brings the ascending limb filtrate from 300 mOsm to 200, while the ECF becomes concentrated. The descending limb and ECF equilibrate, and you're left with an ECF and descending limb osmolarity that has gone from 300 mOsm to 400. This gives you the state represented in frame (1). The increase in ECF and descending limb filtrate osmolarity that is caused by active transport of solutes from the ascending limb is called the single effect.
When fluid moves, 300 mOsm filtrate flows in from the glomerulus, replacing the 400 mOsm filtrate at the beginning of the descending limb (which equilibrates with the ECF), but 400 mOsm filtrate from the end of the descending limb flows around the hairpin and continues along the ascending limb, giving you the state represented in frame (2). This new state is the result of the flow of fluid.
Now the single effect operates on this new state. At each point along the ascending limb, active transport of solutes dilutes the filtrate in the ascending limb and concentrates the ECF, which equilibrates with the filtrate in the descending limb, giving you the state represented in frame (3). Here you can start to see an up/down gradient establish. Continue these steps, and you can see how a substantial gradient can form.
Countercurrent exchange
After being presented with countercurrent multiplication, students will often ask how it is that solutes and water equilibrate horizontally in this diagram (i.e., between the descending limb and the ECF), but not vertically. This is a different question, and is where you start to need yet another compartment, the blood in the vasa recta. This mechanism is called countercurrent exchange, but is the answer to another question (how come the corticomedullary gradient doesn't dissipate?).
Original paper
In addition to physiology texts (e.g., Costanzo Chapter 6), you can read one of the most important original papers supporting this mechanism. Originally published in 1959, it was reprinted here in 1997 and available for download. See if you can follow the connection between the data and this mechanism.

Water in the glomerular filtrate moves out of the descending loop of henle due to the higher concentration of salt in the medulla. The higher concentration of salt in the medulla also moves down it's concentration gradient into the descending loop. The salt is pumped from the glomerular filtrate into the medulla in the ascending portion of the loop of henle. Salt, water and additional molecules can also be reabsorbed into the body in the distal convoluted tubule and collecting ducts and can be regulated by hormones to control salt and water excretion and retention which can affect blood pressure. The proximal convoluted tubule reabsorbes an increased amount of necessary molecules such as 100% of glucose and amino acids.


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What do memory cells actually do?
So I know that memory cells "remember" the most efficient way to kill a pathogen should it show up again... but what is the mechanism by which memory cells become activated by the second contact with a pathogen? How do they interact with the other immune cells to enhance immunity?
For example: phagocytes engulf pathogens and plasma cells release antibodies, but what do the memory cells actively do?

I think memory cells will efficiently do clonal expansion so that it can produce immune cells which can actually remove the pathogens quickly compared to the first time as it now remembers the method it used before.

Can you provide evidence for why you think this? Unsourced or opinions can/will be challenged.

Sure, I read it from Immunobiology: The Immune System in Health and Disease. 5th edition.

On the first entry of a pathogen a division of B cells produce memory cells that remember the details about the pathogen to protect the body during it's next entry.
On the second entry of pathogen, the memory cells get activated and activate the remaining cells of immune system to kill it.

This is basically a part of Secondary immune response which lasts longer than primary immune response( the response where the memory cell encounters the pathogen for the first time).

The process of activation of memory cells is still unknown and scientists are working on it.
The Secondary immune response makes a person immune to various diseases. That's why, a person surviving disease like Chicken pox, Small pox, Measles, etc. gets lifetime immunity to such diseases.
The concept of vaccinations are also based on the concept of "memory" of our immune system.

One the first entry of a pathogen some B cells produce memory cells that remember the details about the pathogen to protect the body during it's next entry. The process of activation of memory cells is still unknown and scientists are working on it.

Edited the answer. Hope you understood the answer.


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How are bubbles formed and how do they make dough rise in bread?
So we took in biology that carbohydrate is broken into $\ce{CO2}$ and ethanol. But all I see in my mind here is that since gas is inside the dough then the gases will try to get out expanding the dough and rising it and I know that ethanol will rise as it is baked. However I am not sure how and why are bubbles formed in the first place or how they're related to this at all and does the ethanol taste stay in bread or is it completely removed once rised?
I heard on another resource that;
"It is because air bubbles get stuck inside, and when the bread bakes, the holes appear."
How does bubble getting stuck inside lead to holes appearing? it is confusing me.

For a yeast bread, the yeast is consuming sugars in the dough and producing CO2.  Kneading the bread causes the gluten in wheat to link up and become elastic, sort of like rubber.  So the CO2 makes lots of tiny little balloons in the dough.  A similar process takes place with non-yeast breads (and cakes &c), except that the CO2 comes from baking powder or soda.  AFAIK the ethanol really isn't a big factor in rising.

So it is because of the immense collision of CO2 into the bread it breaks and goes up? If so how does that piece it collided with go away?

@jamesqf — Please follow the instructions in the comment box. Do not use comments to answer questions. This negates the model on which SE is based.

Anybody competent and/or interested in this matter will answer the question on finding it, until then you need to have some patience.

@David: If I was a food chemist, I would write an answer.  Since I am not one - just a person who bakes, and takes a reasonable interest in how the process works - my comment is simply directed at helping the OP find an answer elsewhere - something that is all too often  hindered by those poorly thought out instructions.

@jamesqf You don't need to be a food chemist! You could write your comment as an answer, I'd say

@jamesqf — The instructions are not poorly thought out. They are integral to the SE model, as you will see if you re-read the introductory tour. Their importance — and unfortunately frequent violation — is why they are emphasized in the comment box. One pays nothing to use this site, so one should abide by the rules or find a different one with a model that one prefers. Please try to help make the site better.

@David: Perhaps you (or whoever wrote those rules) might learn something from that frequent violation, which is that many people who participate here do so despite those rules, and the model they try to enforce.

What I have learned from users who answer questions in comments is that text injunctions are insufficient if others are seen to be ignoring the rules with impunity. Hence the need for human intervention. The SE model states that “moderation starts with the community itself”. I did not invent the rules, nor am I a moderator, but I understand their purpose, and I implicitly agreed to them when I joined SE. Those who wish to understand the SE model and why it differs from other models should watch this YouTube video presentation from the founder of SE: https://www.youtube.com/watch?v=LpGA2fmAHvM.


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What's the (or some of the) minimum(s) amount of atmospheric carbon dioxide needed by plants?
We currently have a problem of increasing $\ce{CO2}$ in the atmosphere.  But assuming we find a way to carbon sink it, what is the minimum $\ce{CO2}$ we need to leave in the atmosphere to provide a source for plants to photosynthesize?  I'm assuming this may vary per plant, and that we could choke plants so they're less productive - but at some point they will starve to death if we remove too much $\ce{CO2}$.
Where does this point lie?
Approximations, or a specific data point (say for one plant, or one type of plant) would be an adequate place to start.
Current atmosphere composition is $\pu{0.035\%}$ carbon dioxide.  In the past it has been higher (has it ever been lower?), which in theory has resulted in higher plant growth - but I've seen some contradictory statements about higher Carbon Dioxide.
(related: What is the effect of a pure-oxygen environment on a plant?)

The Carbon Fixation wiki page will interest you, especially the discussion about C3 and C4 carbon fixation.

In northern BC and Yukon with the increase in CO2 plant growth has accelerated over the last 40 years from my personal and others observations. The result in some values is thicker higher 'buck brush'.

There is no one answer of "how little".  Each terrestrial plant depending upon its type has some minimum below and a maximum above which it could not survive over a sustained time at that level. So it's not just "how little" but "what plant" and "for how long" until it dies, rather than just going dormant or simply not growing.  But the question doesn't involve carbon dioxide alone, there are other conditions (amount of sunlight, temperature, humidity,  annual rainfall, soil quality, air quality) impacting any lower and upper limits.  Deriving some answer for some plant in a closed system like a tube in a lab is one thing.  In nature, the conditions leading to some extreme carbon dioxide level (like either 50 ppmv or 5,000 ppmv) the conditions themselves just to get there likely would kill a plant before even reaching the level of carbon dioxide.
It's rather immaterial to the question this assumption that there is some problem in current atmospheric concentrations of carbon dioxide. Problem to what, how and why?   Yes, carbon dioxide levels rose in 2017 by about 2.48 ppmv, to 407.54 ppmv. https://www.esrl.noaa.gov/gmd/ccgg/trends/global.html  There's also a current 0.79°C anomaly to go along with that 408 ppmv level. https://www.ncdc.noaa.gov/cag/global/time-series/globe/land_ocean/12/3/1880-2018   Assuming some sort of a direct cause/effect relationship to the planetary average temperatures solely attributable to this rise in carbon dioxide levels, still asks the question, is that all a problem?  Trying to answer that is another issue entirely though, and also rather immaterial to the question of how little is too little, since it's going up not down.
We can scientifically - by observation and experimentation - establish  both that increasing atmospheric concentrations of carbon dioxide are happening, and that carbon dioxide absorbs and emits in the infrared.  We can also show the global average sampled near-surface temperature and trend are up.  However, like questions of what level of carbon dioxide is not enough for plants, what we can't observe or experiment upon - on the actual Earth's planetary weather systems - is maintaining everything else and seeing what occurs with a given amount of one or more greenhouse gases that is higher or lower than the current amount.   We can only experiment in non-Earth conditions or model scenarios on computers.  Simulation, given certain other assumptions.   This makes it difficult to do a lot of things, including calculating in the atmosphere when there's not enough carbon dioxide for plants.   In large part, this is because it's not possible to control most of the hydrosphere, or the sun, or the many other factors impacting plants and how well or badly they fare.
That said, there is only one period in Earth's history where the conditions are like they are now, and that is now.   In the existing conditions, it seems unlikely that - regardless of how much or little warming it causes - there is any way to reduce the amount of carbon dioxide in the atmosphere in any realistic timeframe to something lower than it was in 1880 (proxy, ice cores, 282.9 ppmv https://sealevel.info/co2_and_ch4.html)
A question like "at what level of carbon dioxide in the Earth's atmosphere do plants start to die" is a tricky one, because the conditions required to get to 250 (or 200 or 150 or 100 or 50 or 0) in the atmosphere would most likely require an atmosphere that would have lost much of the greenhouse effect to get there. Essentially plants (and just about every animal that would miss eating them) would be hit by extreme cold before they were hit by carbon dioxide starvation.
Although the best answer to these sorts of questions might be found in the ice core proxies, in that during the last million years or so, the atmosphere has not been lower than about 180 ppmv    https://carboncycle.princeton.edu/research/atmospheric
In a controllable laboratory environment, different plants have different levels of carbon dioxide at which they won't grow, go dormant, or die. These are created conditions though, artificial, unnatural.  On the Earth, in the system that actually exists, those levels of any of the greenhouse gases appear unreachable in a working biosphere anywhere near like the one we have. There are too many variables to just consider carbon dioxide, because it can only be experimented upon in a closed system that is unlike reality.

Your answer does not really address the original question. Can you please [edit] your answer to add points relevant to the question? Otherwise your answer may be deleted.

Minimum  concentration in PPM to support plant life varies from 185 ppm to 225 ppm. We are at 433 ppm at the moment. Prior to this Ice Age cycle that started about 3 1/2 million years ago the PPM Norm was between 900 and 1120 ppm. For reference if anybody is interested in knowing where we are at prior to man cause global warming we were at 240 to 250 ppm.  Yeah when I discovered with the plant life minimum was and then where we were at it scared the shit out of me too I.

Welcome to BiologySE! Can you list some references for those values? I'm not familiar with them, and we always appreciate references.

Actually we are only at 405ppm (Source: NOAA https://www.esrl.noaa.gov/gmd/ccgg/trends/global.html)


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If you start with 1 cell how many are at the end of meiosis?
If you start with 1 cell how many are at the end of meiosis?
Can someone help me understand the process of what happens to the cells in the process of meiosis I and II

Welcome to the Biology Stack Exchange. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Please ensure your post is formatted correctly as well.

Meiosis is a process of cellular division involving two consecutive cellular divisions. Unlike the other process of cellular division-mitosis it leads to twofold decrease in the number of chromosomes in the cell, e.g. there are half as much chromosomes in the nucleus of the cell as there were before the meiosis. But the cell undergoes 2 consecutive division so the answer to your question is 4! There are 4 cells at the end of meiosis.
There might be what some people would consider (exceptions) in some cases like in the mammalian ovogenesis (this is the production of egg cells) where the products of one of the cells produced by the first division don't develop and there isn't second division so the total number of cells is 3 but this is considered an exception, so the proper answer to your question is still 4.

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

What do you mean by that comment?

This question can be easily answered by a search on google.Please avoid writing answers for questions that do not have any research effort because they are off-topic


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Why females don't have much sexual desire when compare to males?
I read this Wikipedia article about Playgirl, It is made especially for females. but Its Spokesman Daniel Nardico revealed subscriptions are generated more from males.

In a February 2010 interview with the Associated Press, Playgirl
  spokesman Daniel Nardico stated that he considers the magazine
  appealing to both men and women, although the audience is
  predominantly male

I found another source here to claim,

They did not find a single study that showed that women had a higher    sex drive than men.
But Majority found that men had higher drive than women.

Why females don't have much sexual desire when compare to males?

Welcome to Biology.SE. In order to ask Why, one must first show that the claim is true or instead start by asking whether the claim is true, otherwise the question must be closed as opinion-based. I am afraid that a wikipedia article about Playgirl reporting an interview with a nightlife impressario is most definitely not an evidence that females have less sexual desire than males. I am voting to close as off-topic because it is opinion-based

In fact, if you just google Do females have more sexual desires than males? you'll get plenty of hits like this one, which although they don't cite a peer review paper rather suggest that your claim is wrong.

Where did you get the hypothesis from that more male subscribers for a magazine equals less sexual desire for females?

@Remi.b I added another source link to claim it, still is it closed?

Males often have more desire from a distance, but up close they turn cold. The opposite applies to females.

@The two added quotation seem to come in opposition.... I am definitely not convince yet that it would be true that females have less sexual desires than males.


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Are primary lysosomes same as vesicles budded off from golgi bodies containing hydrolyzing enzymes tagged with mannose-6-phosphate?
SO, as far as I understand, lysosomal hydrolyzing enzymes are first synthesized as proteins in rough ER and then they are budded off from the ER. The vesicles containing those proteins reach cis golgi and then they are properly folded to proper hydrolyzing enzyme but they are tagged with mannose-6-phosphate at this point, so they font have the ability to hydrolyze molecules just yet. In the mean time, some molecules can be engulfed by the cell and and these enter the cell as a membrane bound vesicle (endosome) containing proton pumps in its membrane which maintains an acidic environment inside the vesicle (which matures to late endosome). Vesicles containing hydrolyzing enzymes now move to those late endosomes and fuse with them. The low pH cleaves the mannose-6-phosphate tag from the enzymes and they become functional thus late endozome matures to lysosome.
The definition of primary lysosome says it is that lysosome that directly buds off from the golgi bodies and secondary lysosome is that lysosome which gets formed when primary lysosome binds with a vesicle and hydrolyse its content.
So are primary lysosme and those vesicles same?

What is the question here? If you want a fact check,  try wikipedia or if you are more academically inclined try searching on pubmed.gov for articles about lysosomes.

Flagged question, as this is more of a fact check, which the asker should perform personally.

The question is clearly visible at the top of the page. Then I mentioned what I know about them so far. Had wikipedia been an authentic source of information, I wouldn't have asked here. And I could not manage to find anything that answers my query in pubmed as well. Stop flagging my question for no reason, questions get flagged if there is no attempt of research has been shown. When it is shown, it becomes fact check. What do you want me to do?

Sorry for my french, but essentially you are asking a yes/no question, which you should be able to check yourself. I see that you have edited your question slightly, but the remain the same.


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A little help understanding DNA supercoiling
I am studying molecular biology from Lewin's Genes XII and got confused in the supercoiling topic. Since then I read from several other sources and so far understood the following. However, I can't seem to connect the dots. A bit of help in connecting the dots would be greatly appreciated.
So these are the stuff that I understand so far

Supercoiling is coiling of already coiled double helix
Positive supercoiling overwound the DNA (increase the number of turns thus decreasing the number of base pair per turn making it more twisted)
Negative supercoiling underwounds the DNA
Linking number is the sum of twist and writhe, twist is basically number of turns and writhe refers to the number of supercoil. It remains constant as long as phosphodiester bonds are not broken
unwinding DNA at replication fork results in positive supercoil downstream

Now coming to the confusion

In the diagram we can see that negative supercoiling has taken place. Twist value has gone up and to compensate that (to keep the linking number constant as no phosphodiester bond has broken in this case of cccDNA) six negative supercoils have been introduced.
All the books clearly mention that negative supercoil is something that underwounds the DNA resulting in less turns with more base pair per turn. But in this case it is clearly seen that the number of turns have increased (from 36 to 42) and to compensate that -6 supercoil is introduced. So here negative supercoil has resulted in over wounding instead of underwounding
similarly, from the linking number equation > Lk = Tw + Wr, If there is positive supercoiling (i.e., Wr is positive) the Tw (twist value) will go down to keep linking number constant. So, the statement saying positive supercoil wound overwound the DNA is not matching at all. shouldn't positive supercoil increase the Tw as well (I understand mathematically it is not possible because then linking number would change, but all I'm saying is that I fail to connect the concept that says positive supercoil overwounds the DNA (more twisted) with what I see in the equation i.e., twist number drops and only writhe goes up.

After studying this topic a bit more I came to the conclusion that supercoiling itself does not overwound/underwound the DNA any further that it already is. Supercoiling just relieves the stress introduced after DNA gets further twisted in the first place, it relaxes the DNA by decreasing the twist back to normal (10.4bp per turn just like normal relaxed B-DNA) (in case of positive sueprcoiling and vice versa for negative) and the extra tension that made the DNA twisted in the first place now increases/decreases the writhe for positive and negative supercoiling respectively. The authors might have considered a DNA molecule with higher writhe value also a more wounded form of DNA that's why they used the term 'overwound'
Please correct me if I am wrong


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Why are the first and last amino acids of an alpha helix not hydrogen bonded?
I am studying protein structures and in alpha helix I found out that one amino acid residue's carbonyl oxygen is linked to the nitrogen of amino group of 4 residues ahead.. However the first and last amino acids are not H bonded.. My question is why so? Shouldn't the first amino acid's carbonyl oxygen 5th residue's amino nitrogen like every other one.

Hydrogen bomd  forms between alpha  carbonyl group of 1st peptide bond with alpha amino group of n+th  amino acid residues away towards c terminal direction. Each and every amino acid residues in alpha helix should be inolved in H bonding it is the first 4 alpha NH2 group and last four alpha  carbonyl groups which are not involved because for first four alpha amino group there is no preceding carbonyl groups and also for there is no alpha amino group for last  four carbonyl groups.


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Understanding PAM and BLOSUM matrices
This question might be silly but I need some clarification.
I'm slightly confused about if there are multiple PAM and BLOSUM matrices? Is there a different matrix for each sequence?
My understanding is that PAM and BLOSUM are substitution matrices that are used to demonstrate how similar a sequence is to other sequences by seeing how many iterations of the matrix multiplication are needed before being able to achieve a "similar primary composition". Is this correct?
As I've understood it this means that if I want to compare 2 sequences together I can just this iterative calculation until the relationship between my target sequence and my initial sequence is maximized and then see if that similarity is enough that I can say they are closely related.
This is all assuming there is one standard PAM250 and BLOSUM62 matrix which I'm assuming are calculated from information derived from all information collected on protein sequences.
So when using PSIBLAST to search for similar sequences using BLOSUM matrices does it calculate similarity scores using BLOSUM matrices and then if this score is above a certain threshold it returns that sequence. If you do this for multiple iterations then what is the next input that it uses?
Thanks
EDIT: I think some of the reason for my misunderstanding is that I'm not sure why there would be one single matrix which can be used to determine the "resilience" of a particular amino acid in general. Isn't the "usefulness" or that amino acid dependent on the function of the protein? In that case shouldn't there be different substitution matrices for different proteins? Is this why PAM matrices have difficulty and is this semi-solved by using BLOSUM matrices which use blocks and so can capture when certain "blocks" of amino acids correspond to particular functions and are therefore seen together a lot and are resilient to change in that way? It still seems a bit strange to lump them together in this case.

There are multiple matrices. The matrices scores various mutations slightly different and the use of them depends on how big the evolutionary distance is expected to be among the sequences.  (https://en.wikipedia.org/wiki/Point_accepted_mutation)(https://en.wikipedia.org/wiki/BLOSUM)

@JeppeNielsen There are multiple matrices as the matrix is generated based on the sequence that I'm querying? Or there are a few standard matrices that are used depending on the type of query?

Possible duplicate of Scoring matrices (BLOSUM & PAM) in BLAST and other sequence-comparison programs

Possible duplicate of https://biology.stackexchange.com/questions/49036/scoring-matrices-blosum-pam-in-blast-and-other-sequence-comparison-programs. Please search for other questions on a topic on SE Biology. BLOSUM brings up several hits.

@David Sorry, I don't think it's the same thing. I came across that topic and read it multiple times but it doesn't answer my question.

That answer only states how they're calculated not what data is used to calculate them nor does it discuss differences between matrices when using different query sequences, or intuition behind "lumping them together" which is what I'm after :/

The Wikipedia entries describe the data used for these matrices. As already commented, many pre-existing Protein (not DNA as in your question) sequences are needed and used to get a meaningful matrix. No, it isn't perfect, but your intuition is wrong — it works well enough. No, you can't use a matrix from two sequences, and especially two you are trying to align with a program that uses a matrix. Yes, you can modify standard matrices to get position-specific matrices as you perform multiple alignments of many sequences you already know are similar (see docs for Clustal).

Not at all. I don't answer questions in comments, so if others don't vote this as off-topic, I'll post a proper answer next week. (But anyone else is at liberty to spare me the chore.)


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Identifying Fossil
Few days ago I found this stone with fossil near 6 centimeters. Can anyone identifying it.
Location: Europe,Bulgaria, Elena


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The link between muscle mass and muscle strength and how to train for each
I'm getting into my fitness and am beginning to see an increase in muscle mass. However, I look at people like Bruce Lee, Elliott Hulse, Mohammad Ali and Wim Hof who are capable of incredible strength but do not look as "buff" as people like Arnold Swarzenegger. It is clear that an increase in muscle mass does not necessarily lead to an increase in strength.
How is training for strength different to training for mass?
To add a new angle to this question, is there a correlation between the two?

FYI Correlation between muscle size and absolute strength

I'm voting to close this question as off-topic because it is better suited for fitness.SE.

I think this is perfectly at home in the biology stack exchange considering it conscerns biological functions.

Also: How does muscle size relate to strength?


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Has human evolution currently stopped?
Due to the advent of social networking and dating sites, it is now possible for almost anyone to find a potential mate. Therefore, there is not as much of a pressure based on physical characteristics or even intelligence anymore. Society does not present the same pressures as was historically present in nature to find food and avoid being killed by predators and potential mating rivals. Almost all alleles regardless of their characteristics are passed on to the next generation through someone or another and attractive traits are no longer chosen above deficient ones. The only exception often being conditions such as dwarfism, Down Syndrome or Parkinson's Disease where the recipients of disadvantageous alleles choose to remove themselves from the gene pool.
Therefore, does this mean that human evolution has been halted due to an absence of natural selection?
My question differs from "Has human medicine stopped humans evolving?" because my post focuses on societal and cultural changes as opposed to medical changes.

"My question differs from "Has human medicine stopped humans evolving?" because my post focuses on societal and cultural changes as opposed to medical changes."
Still a duplicate because the answer is still that humans continue to undergo strong natural selection, so it doesn't matter what you speculate is preventing natural selection, it isn't stopping natural selection. If this question is considered not a duplicate, you could then ask if Sugar-frosted Wheaties are stopping evolution, and then if bleached hair is stopping evolution ... doesn't matter since the premise is wrong.

If the premise is wrong then respond by answering. Just because 2 + 3 and 7 - 2 have the same answer they are not the same question.

The questions are different clearly

On top of the two posts marked as duplicate, you might also want to consider the post Is there evolution in humans since the first homo sapiens sapiens

No charlie they really are not, the question boils down to are humans still evolving and the answer is yes. All the speculation does not change the fundamental question. It might not be an exact match to the two marked questions but Remi's linked question is identical, even to the timeframe.

"Due to the advent of social networking and dating sites, it is now possible for almost anyone to find a potential mate." - Citation needed.

Evolution is an attribute of complex adaptive systems, it is a mistake to consider it as just a biological phenomenon. Human physiology, culture, society, economics and the environment, and so on, are all examples of complex adaptive systems, and interdependent (actually not separate). Evolution is inherent in the system, it never ceases.


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Why does the brain produce cannabinoids?
I've been reading lately about the brain producing cannabinoids. I was introduced to this idea by the Wim Hof Method which has been shown to increase the amount of cannabinoids (that is, compounds simulator to those found in cannabis) produced by the body.
Could anyone enlighten me on why the body naturally produces cannabinoids in the endocannibinoid system other than the shallow explanation that they have any anti inflammatory effect?

The intention of my question was "what purpose do cannabinoids server in the body?" Why does the body produce them?

I will do, much appreciated.

It's interesting to me that cannabinoids, opioids, etc are naturally occurring substances in the body; it's a change of perspective for me. I've always believed those substances to be foreign substances in the body as opposed to something that's always meant to be there.

It's important to note that the foreign agonists are often either much more potent or in much higher concentration than the endogenous forms, which is in part why it was easier to identify those agonists first. Another type of neurotransmitter that is very common in the brain is glutamate, but even various ionotropic glutamate receptors are known as "AMPA", "NMDA", and "kainate" receptors. They all respond to endogenous glutamate, but they also respond to those other molecules selectively.


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Why did many species of Homo and their ancestors evolve in East Africa?
One thing I find interesting about the theory of evolution is the idea that Homo Erectus and Habilis evolved in Africa, began to spread around the globe, then was superseded by Homo Sapiens Sapiens which also evolved in Africa. Why did the vast majority of Homo species evolve in East Africa first?  What was it about Africa which encouraged speciation more than other areas?

Neanderthals probably evolved in Europe, not Africa, raising from a common ancestor that was present in both regions.  See The origin of Neandertals

Hi mate, thanks for this. Didn't know Neanderthals likely evolve in Europe, this changes my perspective somewhat.

Denisovans and floresiensis also probably evolved outside Africa. But all had a common ancestor that was African, and the division into "Homo" vs other groups is a little arbitrary

because of the trees, lizards evolved on the ground, and the apes lived on the trees, it wasn't until the extinction of the dinosaurs, that some of this apes returned to the ground and spread in the world. Africa was the safest place on those times.

Interesting idea, can you back this up with any studies? Don't think apes and dinosaurs had any overlap, first mammals were roughly 60 million and dinosaurs died out at a similair time. Also trees wouldn't explain the speciation, trees are found everywhere.

I know our shared ancestor with the opossums is contemporary to dinosaurs, but opossums are terrestrials which contradicts with my theory, its more likely that after dinosaurs went extinct other mammals became his predators and that's why they climbed the trees, maybe those predators existed in Africa only.

The main basis of my question want to do with the original evolution of Homo, but more to do with why East Africa was the hub of many stages in evolution. So as my question details you had Erectus and Habilis evolve in a very small area when they could have evolved ANYWHERE, then you had Homo Sapiens Sapiens evolve AGAIN in East Africa, even though there were Neanderthals in Europe too that could have evolved instead.

its more likely that homo sapiens killed them all, living outside Africa was probably relatively easier, away from danger, while in Africa homo sapiens was struggling to survive after descending from trees. that might be the original reason why many cousins left in the first place.

The question is based on a false opinion but I'll get back to that at the end.
Humans are still evolving

Why did all species of Homo evolve in Africa first?

Humans are evolving all around the world. Evolution is not a thing that stops once we made the arbitrary decision of naming a lineage. When we first named humans, Homo sapiens sapiens, indeed the lineage was living in east Africa.
Humans is a lineage of Old World Great Ape

One thing I find interesting about the theory of evolution is the idea that Homo Neanderthalis evolved in Africa

It would help if you could explain why you find that particularly interesting. It is possible that some falsy teleological view of evolution you may have might push you to make some unexpected conclusion from the idea that first Homo lineages lived in Africa (but might be wrong in your understanding of evolutionary processes). In any case, you can find an very introductory course to evolutionary biology here if you're interested.
If humans were a species of feline, it could have evolved elsewhere (it would look very different to what we currently call humans of course) but humans is a lineage of old world great ape. Old world great ape lived mainly in Africa. There is not much more to say about it.

why Africa did Africa encourage evolution more than other areas of the world?

Africa is a continent. It is big! You can find pretty much any biome in the world in Africa (except toundra and taiga if I am not mistaken). Did the specific location where humans lived in Eastern Africa affect their evolution. Yes, the evolution of a population is always affected by its surrounding. For example, the presence of large game was probably a big selection pressure for cooperative hunting (but you can/could find large game everywhere).
It will be near impossible to answer in the general sense. A lot of things happened in human evolution. Even if you tackle down to a single trait, it will be hard to tell you what would have happened if the world would have been different because it was not. (WorldBuilding.SE welcomes questions like "if it was like that what would have happened?").
Origin of Homo lineages
There are a number of named Homo lineages, some of them have not lived in Africa. This include for example Homo floresiensis.

The reason I described it as interesting is that to my understanding many significant stages in human evolution (the majority: Australopithecus, Homo Erectus, Homo Habilis, Neanderthals, Homo Sapiens) occurred in Africa; however, I'm well aware evolution is occurring all the time. My question was why Africa did Africa encourage evolution more than other areas of the world?

PS, I'm well aware there are exceptions to the rule and certain species evolved elsewhere.

I edited the post to try to address your comment. But I am afraid no one will be able to say much to such question (not so much by lack of knowledge but more due to the semantic of your question). But we'll some others might find more things to see that may be of interest to you


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At what level of relation does inbreeding become dangerous?
Inbreeding within first cousins appears to have an established history of dangers, and anything closer than that relationship also.
However, how distantly related do two individuals have to be for the risks of inbreeding to be in line with having a child with an unrelated person?
Are second cousin children more likely to have children with defects? 3rd cousins? 4th?

Are you talking about interbreeding or inbreeding? You are using both words. I would assume you're talking about humans, right?

@Remi.b yes I am talking about humans

And I'm talking about inbreeding

Possible duplicate of Is marriage with half-cousin's daughter more risky than marriage with others?

Any level of inbreeding increases the risk of genetic disorders, but one single instance is not dangerous. The issue appears when inbreeding becomes the norm and goes on and on and on. Even two siblings could have a child with only a small increase in the percentage of having a genetic disorder. Now, after 50 generations of doing that, it becomes really bad...


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Looking for the exact text and attribution of "Evolution does not wait around" quote
I am looking for a reference for a quote that roughly said:

Evolution does not wait around. Either things happen quickly or not at all.

I thought the quote was from Carl Woese but I have gone through a number of texts from him that I have read in the past and could not find it, so likely the quote is from someone else entirely.
Addendum
I am increasingly certain that the quote is from Christian de Duve. For example, Nick Lane writes about him in "Life Ascending":

The Nobel laureate Christian de Duve, equally eminent, argues altogether more thrillingly that the determinism of chemistry means that life had to emerge quickly. In essence, he says, chemical reactions must happen rapidly or not at all; if any reaction takes a millennium to complete, then the chances are that all the reactants will simply dissipate or break down in the meantime, unless they are continually replenished by other, faster, reactions. The origin of life was certainly a matter of chemistry, so the same logic applies: the basic reactions of life must have taken place spontaneously and quickly. So life, for de Duve, is far more likely to evolve in 10,000 years than 10 billion.

This paper by de Duve certainly argues the point in question, however, it does not contain the quote itself.
I suspect that the quote may come from his book "Singularities", but I don't have access to the book at the moment to confirm.

Hi & welcome to Biology.SE. On this site, there's a requirement to show evidence of an attempt to answer the question, e.g. a quote and a link. Granted, the quote part is hard here, but "I've looked everywhere" isn't evidence, unfortunately. I did DV, not for the question but for an impersonal reason: the quote is nonsense, and will be difficult to find even though nonsense is all around us in media. Evolution is continuously occuring. If you were given this concept to defend in a debate, I do wish you luck.

@anongoodnurse I asked for a reference for a quote I am struggling to remember, not opinions on evolutionary theory. While I am new to this stackexchange site, I am surprised that the opinion expressed in a quote constitute sufficient grounds to downvote a question looking for said quote.

@anongoodnurse I have added further evidence of my continued search to the question. I warmly recommend you read the linked paper. You may be surprised by the breadth of opinions expressed by experts in this matter.

This is a science site and the quote is ridiculous. Hover over the downvote button and you'll see the reasons suggested. Lack of research is one, not useful is the other. I can't see any usefulness in asking for the author of a nonsense statement. Please enlighten me if I'm in error. I have no argument with the new quote, in fact I agree (no surprise there). But it's not about 'evolution occurring quickly or not at all'. It's not even about evolution, not at all. So, imo, no real reason to change or delete my comment or my vote.

In principle, this is a question for SE History of Science and Mathematics. In practice, my recent exploration of that site suggests that only a few biologists frequent it. If the original quotation was in French, you may have a hard job finding it.

@David Thanks for the advice and warning. Also, the idea that the original quote may have been in french is an excellent one. I will widen my search accordingly.


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Why social animals attack odd members of their own group?
Some social animals are known for attacking odd members of their own group, for example, chicken:

If you have a large group of one type of chicken, they will usually gang up on the one or two others that do not look like they do. They recognize color differences the most and will beat up on the odd chickens in a group.

Of course the same behavior is most commonly observed in humans, where any difference can be a reason for aggressiveness.
Why this behavior developed and still exists and how it is called?

The same article also states that "being kept in too small of an area can also create aggressive situations in chickens of the same breed". This happens with many other animals, including humans. Perhaps the behavior you relate happened in an isolated area? In this case, kin selection theory predicts that the first attacked individuals will be those that do not look like relatives.

@Rodrigo, as I understand it, space constraints just increase aggressiveness, not cause it.

I couldnt find specific terms for aggression more than territorial disputes, hyerarchy disputes, persecution, xenophobia. It doesn't seem to have been studied as a general phenomenon. I found something about malawi fish attacking individuals of the same color. Wild chickens don't differ much genetically, and a persecuted albino/mutant can normally leave the flock. to the chickens, the mutant perhaps looks unwholesome and they are trying to chase it away, except it can't escape. Reasons why are very interesting and hyper complex and take several pages to list.

@comprehensible, can you at least provide a summary of these reasons, so I would know what to search for?

In ethology, aggression is part of what we call agonistic behavior. Yes, space constraints increase aggressiveness. Hens do attack each other in order to establish an hierarchy (the pecking order). Maybe the conditions in which the observations of your source were done help to explain what was going on. I think it may be a mix of territoriality, kin selection and restricted space.

Persecution is not a term often used in zoology, compared for example to the notion of social exclusion and hierarchy disputes/social animal hierarchy. That is because humans incarcerate animals which would otherwise flee to safe distance from the group if they are attacked. Wild Mammals, birds, fish, other animals with free movement can normally get safe distance from an aggressive group in order to be safe from persecution.
Fish and insects/island animals sometimes have restricted ranges, and "social exclusion of a mutant" - studies are difficult to find and perhaps won't give masses of information to know why it happens, for categorization and prevalence of different reasons.
I found only one research on social aggression based on appearance:Aggressive biases towards similarly coloured males in Lake Malawi.
Useful related terms for further research for your question are i.e.:

"social exclusion mutants traits aggression"
"social exclusion zoology"
"social exclusion injury zoology"
"social exclusion zoology mutation"
"hyerarchy disputes appearance zoology"

It's an interesting notion for research that you have found, for which a lot can be written, because it gives a complex range of potential reasons for the given behaviour: warding off a contagious individual, warding off a tribe from far away that could displace the current group, inability for the brain to average the mutant's appearance to associate with it, habituation of species to a type of social companion since their birth (i.e. birds sometimes think they are humans)
And so a research requires a broad understanding of juvenile establishment of appearance recognition of other individuals of the group, i.e. where humans search for an average appearance compared to the social group, and chimps recognize close relatives and mate with the most distant, chickens can adopt humans... and animal behaviour towards an ill individual, it's difficult and takes a while to gather actual sci documents for.
When you have found all the closest related research, the given write up would be very fascinating!!! i hope you can search the given topics and give a summary of some previous examples of vaguely related research.

Thanks, I appreciate your answer. I've upvoted it, but I'll leave the question open for everyone to contribute, if you don't mind.


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What's the purpose of segregating a virus from the blood and growing it in the lab?
I heard that the scientist in Australia found a way to segregate the 2019 NovCoronovirus from the blood. Does this mean they are one step closer to the cure? Why is virus segregation crucial in finding a cure for a viral infection?

Isolating virus particles is important for accurate genomic sequencing, which in turn enables study of mutation rates and determination of hotspots, locations in the genome where mutations occur at higher rates:

“Sorting individual viral particles makes it possible to identify and sequence the genomes of viruses one by one,” states Òscar Fornàs, head of the Flow Cytometry Unit of Pompeu Fabra University and the Centre for Genomic Regulation.

Researchers attempting to create vaccines need to know this information about the viral sequence, in order to make a functional vaccine:

Dr. Corbett and others had studied the spike proteins on SARS and MERS viruses in detail, using them to develop experimental vaccines. The vaccines never made it to market because SARS was successfully contained with public health measures before the vaccine was ready and preliminary human trials for the MERS vaccine showed success last year.
But the scientists had a method for developing vaccines that could help them fast-track production for the new coronavirus. They used the template for the SARS vaccine and swapped in just enough genetic code that would make it work for the new virus. “I call it plug and play,” Dr. Corbett said.

Characterizing how quickly a virus mutates, and where, can decide the effectiveness of a vaccine.
In the United States, for example, this year's batch of influenza vaccine did not match up well with the strain of flu virus that ended up becoming dominant:

An unusual viral strain is dominating flu activity across the United States and may be one reason for the severe infections in children so far, according to a new report from the Centers for Disease Control and Prevention, and this season’s influenza vaccine is not a close match for the virus.

There are limited resources to allocate to vaccine development. Faster and more accurate sequencing can help with a more targeted and effective response.

It is also important for testing treatments, developing diagnostic tools, and even just determining what kind of virus it is, sequencing a RNA virus is quite different than doing so on a DNA virus for instance.

2019-NCoV was first cultured by a Chinese group, as published here on January 24. China has not shared samples, but did share sequencing data in the linked paper and via GISAID. The Australian group at the Doherty Institute hasn't published yet, but did put out a press release today (January 29), and appears to be the first group outside of China to have cultured 2019-NCoV.
Viral isolation, and in particular, culture, is an important, and often difficult step in characterizing a novel virus. Once characterized, viral culture serves as a gold standard for diagnosis. Generally speaking, the ability to grow virus in cell culture allows for a broad range of pre-clinical studies that can lead to clinical advances including prevention, diagnosis, and treatment. Consider how difficult it may be to study a pathogen if you are not able to manipulate it in a living culture. You can read about this in Murray Medical Microbiology, Ch 50. This article, which does not require a subscription, may also be of interest. The article describes a variety of historical and modern methods, but also includes some discussion about the use of viral culture.


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Bird diversity and the avian flu
From Learning from the Octopus 1 (p. 201):

A complimentary line of defense would be to lower the chance of infection by lowering the prevalence and virulence of diseases…just keep the variability of nature intact…West Nile virus increases its prevalence when bird diversity declines.

and on p. 212:

A high diversity of bird species has recently been shown to be a key factor in reducing transmission of some diseases such as avian flu.

Why is this so?
What does bird diversity have to do with reduced disease transmission?

Welcome to Biology.SE. This is an interesting question! I edited the quotations in your question to make them more clear. Could you please provide a reference to the book (authors, a link) you are citing from? Thank you!

Biodiversity is the opposite of monoculture, and we know that one possible consequence of monoculture is disease transmission -- bananas being the modern poster child for monoculture leading to disease spread.
The concept seems to have been most clearly presented in
Schmidt, K.A. & Ostfeld, R.S. Biodiversity and the dilution effect in disease
ecology. Ecology 82: 609–619 (2001)

A community of abundant alternative hosts with reduced competence mitigates Lyme disease risk in this system by decreasing the average infection prevalence of ticks. When alternative hosts have net negative impacts on the most competent reservoirs, via competition and predation, the dilution effect is compounded. We believe this dilution effect to be a general phenomenon of disease ecology because the majority of vector-borne zoonoses are characterized by the fea- tures necessary for it to occur.

There are many articles following up on this one, such as Declining ecosystem health and the dilution effect:

The “dilution effect” implies that where species vary in susceptibility to infection by a pathogen, higher diversity often leads to lower infection prevalence in hosts. For directly transmitted pathogens, non-host species may “dilute” infection directly (1) and indirectly (2). Competitors and predators may (1) alter host behavior to reduce pathogen transmission or (2) reduce host density. ... Our study provides further evidence for dilution effect ...

However, not all agree that this is a general or even a real effect.  For example:

How changes in biodiversity alter the transmission of infectious diseases is presently under debate. Epidemiologists and ecologists have put a lot of effort to understand the mechanism behind biodiversity–disease relationship. Two important mechanisms, i.e. dilution and amplification theories have in some manner made it clear that biodiversity and disease outcome have an intimate relationship.... We suggest a multidimensional approach whereby the same disease system needs to be studied in different ecological zones and then the effect of biodiversity on disease outcome needs to be ascertained. Nonetheless, caution is to be taken while jumping to any conclusion as biodiversity–disease relationship is a multifactorial process.

--Does alteration in biodiversity really affect disease outcome? – A debate is brewing
The book seems to be making the specific claim that biodiversity reduces transmission of avian influenza, and without a reference I can't evaluate that, but I couldn't find any articles supporting the claim. I'd be skeptical about that claim without some good  evidence, because avian influenza viruses are exceptionally good at crossing species barriers, so biodiversity should be much less of an obstacle for them than more species-constrained pathogens.


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Bioenergetics and equilibrium
"The living state is a non-equilibrium steady state to be able to perform work."
I know that a "steady state" is the one in which the rate of energy gain is equal to rate of energy loss. Then how can living beings do work?  Can you simplify it?

Posting text as image isn't a best practice on SE. The same pdf should allow copying and pasting the text into your question ( [edit] ). Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. See this for more information.

Think about why body needs energy to maintain this steady state?

@Tyto alba I understand now. I have removed the image.

The clue is in the non-equilibrium part. The energy is spent to prevent collapsing to the equilibrium, that is indeed death.


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How do transport/carrier proteins rotate during facilitated diffusion?
In my book, it is written that when a molecule binds to the carrier protein then the protein rotates and releases the molecule inside the cell. I want to know how is this possible. Wouldn't the surrounding phospholipid molecules or other proteins hinder its rotation?
EDIT
The rotation axis is in the plane of membrane
Source : http://ncert.nic.in/ncerts/l/kebo111.pdf (page 177, Third paragraph)

Rotation of carrier protein in which axis? is the axis in the plane of membrane or perpendicular to it? If latter is the case then  there shouldn't be any noticeable  hindrance as the membrane is quasi fluid in nature.

@JM97 The rotation axis is in the plane of the membrane.

Please cite the source, or upload a photograph showing rotational axis.

@JM97 I've added the source in the question.

Where does it says that axis is in the plane?

@JM97 Look at figure 11.1 on page 177 and read the third paragraph. Though they've not said that the axis is in the plane of the membrane but you can figure it out yourself. Perpendicular axis don't make sense because then the molecules won't be transported inside the cell

Let us continue this discussion in chat.

The text referring to Fig 11.1 says that the carrier rotates, but this is clearly wrong even in terms of the way the Figure has been drawn: there are arrows to represent a pathway through the carrier, and there is no indication at all that the carrier rotates.

@Alan Boyd Yes. This is confusing.


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Warburg effect in lung carcinoma, the logic?
Outside of 'purposefully' removing mitochondria to diffuse cytochrome C's apoptotic threat, I would assume that lung carcinomas, and their proximity to high oxygen levels, would have the lowest rate of cells entering the Warburg effect. Would this be a correct assumption?
Thanks

As far as I can tell, there are no data to support your hypothesis. Someone correct me if I'm wrong.
There's actually some data to support that aerobic glycolysis occurs in lung carcinomas despite their proximity to oxygen (ref). There's even an article on the prolifertative pathway behind lung microvascular endothelial cells (ref), alluding to this requirement for anaerobic glycolysis in rapid proliferation.
T cells exhibit a similar pathway, switching to aerobic glycolysis in the effector phase where T cells are rapidly expanding (see clonal expansion). The general trend is that the Warburg effect lends itself to the rapid accumulation of biomass, supporting rapid cell division, instead of energy production to support cell survival (ref). You could rationalize it like cancer is already a failure in cell death, and so the cancer cells need to worry more about carbon compounds that support rapid division. There was also a paper by Cai et al. in 2014 that described their hypothesis behind aerobic glycolysis in cancer, whereby the Warburg effect helps tumors resist anoikis and thereby promote metastasis (ref).
It may be that the Warburg effect is a means to a required end for cancer cells, but as far as I know there's is no correlation between proximity to oxygen and incidence of Warburg metabolism. There are papers out there that continue to ask: is the Warburg effect a cause or consequence of cancer (ref? My thought is that cancer cells will undergo the Warburg effect at a given stage regardless of histology or behavior because it's beneficial.


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Identify fuzzy black quarter sized spider with orange on abdomen, in Minnesota
Found this spider on my car in Minnesota near St Paul (USA). Total size including the legs (end of rear leg to end of front leg in picture) is probably about the size of a quarter.

looks like a harmless jumping spider

I'm having difficulty finding another image that matches https://goo.gl/YrXGKm

This appears to be some species of jumping spider (family Salticidae).

[Note that] All jumping spiders have four pairs of eyes, with the anterior median pair being particularly large.

In particular, I believe your specimen is Phidippus audax (Bold Jumper). Specifically, I believe yours is a subadult bryantae variant of this species.

 Source: David Hill 2014
From Wikipedia:

The average size of adults ranges from roughly 13–20 millimetres (0.51–0.79 in) in length. They are typically black with a pattern of spots and stripes on their abdomen and legs. Often these spots are orange-tinted in juveniles, turning white as the spider matures.

Your specimen shares the orange abdomen with connected black "splotches" that leave an orange triangular dot in the middle. Also, notice your specimen has two grey lines on the posterior cephalothorax as well as black/white striped legs. Finally, 20mm is close to the size of an American quarter (~24 mm).

If you get a good look at the front of your specimen, you'll likely see that the chelicerae are an iridescent/metallic blue or green (a tell tale sign of this species and genus).

 Source: David Hill 2014

 More typical coloration (L) vs. bryantae variant (R). [Source: David Hill 2014]
P. audax tends to prefer relatively open areas to hunt and is commonly found in common in fields and grasslands, as well as on fences, exterior walls, and gardens. Finding one on your car, therefore, would not be so strange, especially given that they can jump 10-50x their own body length (Ruppert et al., 2004).
Phidippus contains some of the larger species of jumping spiders in the family, and it is almost exclusively a North American genus.

Specifically, P. audax is common in southeastern Canada, eastern and central United States and parts of northern Central America, and it has become increasingly common farther West.

Citation:
Ruppert, E.E., Fox, R.S., and Barnes, R.D. (2004). Invertebrate Zoology (7 ed.). Brooks / Cole. pp. 571–584

Did you find this e-book [Invertebrate Zoology]? I have been looking for it for ages.


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Wasp using plant fibers in old carpenter bee hole (Indiana USA)
Location: Indiana, USA
Every spring, carpenter bees make a few holes in our exposed porch wood.  This year, we observed a woodpecker removing three 1+ cm white grubs from one of the holes after a week or two (this hole is on the underside of a porch rail).  Interesting enough.  But now, I observed some kind of wasp carrying plant fibers into the same hole, so I guess it is using it as a nest.  Here's a picture of the wasp, and also of the wasp disappearing into the hole with large green piece of grass (at least it looks like grass - definitely a strong flyer).  The hole is about 8 mm across, and the wasp body about 1.5 cm.  Anyone know the species of this wasp?

Update: Here is the apparently completed nest:

Perhaps it is the four-toothed mason wasp.

The plant material now consists of about 30 fibers, looks like a piece of a paint brush sticking out of the hole.

Are you sure both pictures are of the same wasp?  The wasp in the first picture has a white stripe on it's abdomen and the wasp in the second picture doesn't. Another reason that they don't look the same is that the legs of the wasp in the first picture don't look like they belong to the same wasp as the one in the second picture.

@peter Yes, they are the same wasp.  The stripe is hidden in the 2nd picture due to the angle. I have several other pictures of somewhat lower quality than I posted here.  Thanks for your interest!


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Is this a form of *LaetIporous sulfurous*? Tree is in north central Virginia
I found this while walking our dogs. Is this "chicken of the woods"?

This is indeed Chicken-of-the-Woods - and a nice specimen! However, there are multiple species that closely resemble each other, all called "Chicken-of-the-Woods." Based on your location and the tree it is growing on (I am guessing a hemlock or pine from the bark), it is likely Laetiporus huroniensis (see Emberger, 2008), which grows on conifers east of the Rockies (Kuo, 2017).

Fig. 1. An older Laetiporus huroniensus found in West Virginia. image: Django Grootmyers (CC BY-SA 3.0)
If you might eat these in the future, please read this article (Margulies, 2006) concerning potential toxicity. Marley (2010) advises to eat only a small portion and not share your first time, and to not eat those growing on conifers (i.e., this cluster).


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Can anybody identify this kind of plant?
Location: Low Tatras, Slovakia, elevation: 1800 m. Can anybody identify this plant from Slovakia mountains?

Does it look like a young conifer?

I think this is some kind of Hypericum.  In Costa Rica and the Andes there is a high altitude ecosystem called the paramo in which shrubby Hypericum are characteristic species.  The area in your photo looks to be covered with shrubby species, and you are at decent altittude.  Looking at your picture (at full size) the leaves look approximately decussate which is typical of the genus, and also, the stems are ridged which is also pretty characteristic.
There is a good paper here on Hypericum of the Mediterranean region.  It mentions some groups that are shrubby or dwarf but thus far I have not been able to find a species that looks just like your picture.
Update: Possibly it is Hypericum aegypticum which looks about right relative to your picture, esp, the leaf color and size.  Also known to grow at that altitude. Decent picture here plus the one at Wikipedia both look similar to yours.
Update 2: On fresh look, the bases of the leaves for Hypericum aegypticum don't compare well to your picture, but I still think it is a Hypericum.


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Can anyone identify this small shrub? Has white flowers
Small shrub in adelaide south australia garden.

Looks like the common olive, Olea europea.  Cut into one of the fruits and see if there is a stone/pit, which will confirm.  You can search online for images to compare (use the Latin name as your search term).


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Does anybody know what kind of snake is this?
FYI the snake is dead and currently in my freezer, I got it from a guy and forgot to ask what kind it is.

Can you please edit your question and add the location where this snake was found?

I am from Czech Republic, but the snake is definitely exotic, it was a pet.

Is it pictured with the head upside down?

I need a better picture. thaw it, put it in some kind of position so that I can see the back,and give me a length measurement.At least.

This is Orthriophis taeniurus ridleyi, a synonym is Elaphe taeniura. It has a few common names,some are  Ridley's beauty snake,Cave beauty and Cave racer.
https://www.biolib.cz/en/taxon/id310150/
https://www.naturepl.com/search?s=orthriophis+taeniurus+ridleyi2581
https://www.zootierliste.de/en/?klasse=3&ordnung=305&familie=30513&art=21102660
https://www.thainationalparks.com/species/orthriophis-taeniurus
https://en.wikipedia.org/wiki/Beauty_rat_snake
https://www.reptarium.cz/en/taxonomy/Orthriophis-taeniurus/2581


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Unknown aquatic larvae
These critters have taken up residence in standing water in a small terrarium. It is home to several frogs and lizards. If they will coexist peacefully, I have no objection. If they will harm plants or critters I'll have to evict them.

Related: Bug Identification: Tiny Bugs in Fairport NY, What are these tiny, swarming, jumping bugs?, Help identifying tiny jumping bug, Can Anyone Identify This Insect?, Taxonomy: Categorising Collembola, What kind of small insect is this?

Those are collembolans. The common name is "springtail". Several groups of collembola are semi-aquatic. They are not larvae, but adults. There is a nice paper on aquatic collembolans here: https://link.springer.com/chapter/10.1007/978-1-4020-8259-7_36

Not harmful at all.