text:
What is meant by "50% related to sibling" versus "95% related to chimpanzee"?
Obviously I am more related to my sister than to a chimpanzee, so what do these different percentages actually refer to?
Here is my preliminary research:
https://genetics.thetech.org/ask-a-geneticist/siblings-are-around-fifty-percent-related/
https://genetics.thetech.org/ask/ask395/

Related : https://biology.stackexchange.com/questions/61206/how-can-someone-share-50-of-their-dna-with-their-parents-yet-all-humans-share-9

Possible duplicate of How can someone share 50% of their DNA with their parents yet all humans share 99.9%?

The obvious answer is that the two sources you mention are using "% related" in different ways, and ones which are probably not clearly defined, althoug I cannot tell without a full quote (no, it's not up to us to read the references). On the one hand this site is concerned with questions to specific biological problems rather than correcting popular science on the internet, but, as two users have pointed out by their comments, this sort of confusing statement is widespread. A wider question with a more comprehensive answer would probably be useful, but it may take a little time.

50% related to sibling means that, out of the portion of the genome that vary in humans, you share half of them with your sibling. (if you compared total genetic match not just ones that actually vary in humans you are looking at something closer to  ~99.95% match)  Now because because variations are not evenly distributed and your parents likely came from the same source population you usually share more with a sibling, but recombinations has a random aspect, and sex chromosomes have a large effect as well. So 50% would be the average using the most common methods of comparison, and even then it is only shorthand. It is a calculation more than a conclusion, if you are 50% related to your parents and so is your sibling then the probability calculation is [0.5 X 0.5 = 0.25]  Note this is in humans, other animals use different chromosome distributions which can result in different numbers, bees for instance have haploid males making females siblings far more closely related.
95% identical to chimpanzee means out of all the genetic elements only 5% of human ones are unique to humans (or chimps) and not shared by chimps and humans while 95% is shared by both. 95% is a lower estimate because they are using the strictest comparison.
One important thing to consider is there are many ways to compare genetic variance, consider a book as an example, if I switch 2 chapters is that one change, two changes, or hundreds of changes (by the number of letters or words in the chapters). because criteria are different you get slightly different estimates of difference. In the case of the 95% estimate that would be using the "hundreds of differences" method of comparing. Deleting the sentence "Mary had a little lamb" would be 21 changes using this method. Other methods would consider it only one difference since it is the product of a single mutation.

What do you mean by "out of the genes that vary in humans"? As far as I am aware all genes vary (i.e. exhibit polymorphism) in humans. So it is the polymorphisms that you share, rather than the presence or absence of a gene. On which point, could you quote a reference to support your assertion that 5% of human genes are not present in humans — the article the poster cites refers to differences in DNA, not genes, and recent questions related to this suggest the percentage of unique genes is much lower.

No the vast number of genes in humans have no variation, at least ont ones that survive. The human species actually has remarkably little genetic variation. https://www.ashg.org/education/pdf/geneticvariation.pdf As for the 5% thats what the 95% similarirty means, it means 95% is shared and 5% is unique.

The article is not clear about what criteria they are using for comparison so I used the vaguest term available, genes which has both a laymen and more than one technical meaning. I will edit for clarity.

To your second comment — a vague answer is no good for this sort of question. The point is very confusing, given the number of questions about it, and any answer needs to be detailed and very precise. This is a list for "students of biology", not laymen.

You state the vast number (20,000) genes in humans have no variation. Perhaps you would care to comment on this explanation of single nucleotide polymorphisms (SNPs) from the NIH website, in which it states that there are 10 million in the human genome.

there are 3 billion nucleotides in the human genome, 10 million/3 billion = 0.003 that's less than 1%.

Blue eyes, rhesus A-ve, organ donor compatibility. 1 SNP every 300 bases, which is the length of an 100aa gene. No variation?

when did I say humans had no variation in genes or nucleotides? if you want to read more about the low genetic diversity in humans start here. https://www.ashg.org/education/pdf/geneticvariation.pdf

'Yesterday' (i.e. 10.09.18) John commented "No the vast number of genes in humans have no variation, at least ont ones that survive". Grammatically that means "all". It may be that you meant "most" or "the large majority", but, if so, I still dispute that. And you were talking about genes, not nucleotides, here and in the quotation "of the genes that vary in humans" originally queried. I do not "want to read more" but to have you clarify a point in your answer, the purpose of SE comments.  However the article only confirms my contention that most, if not all, human genes exhibit polymorphisms.

Vast number is not the same as all, It is important you understand the difference if you plan on continuing in the sciences, it is a common phrase. My comment is true for genes and nucleotides. I don't know how you could conclude the article says that, can you state what makes you believe this.

Enough. If you want me to explain the grammar, post that sentence on SE English Language & Usage.

Clarifying language is also a part of the process.  "vast number" is a common scientific phrase used in the source literature, understanding what it means is important. Contingent language is very important in scientific literature and if you are having difficulty with it it would explain why you are having trouble with my sources. Asking you to clarify were in a source you see a pece of information is completely normal, I suspect I know what part you are misinterpreting but it would be presumptuous to just comment on it  without clarification.

I said "enough".

The 95% comparison to chimpanzees is within the animal kingdom. That is, compared to other animals, human and chimpanzee genes have a 95% match. The ratio could be as high as 85% between humans and other mammals such as mice.
On the other hand, within the species, Homo Sapiens, you and your sibling may have only a 50% match of genes compared to other human beings. (That would be true if your parents were totally unalike, say European and African. Often, your parents may have some overlaps or even common ancestors. In that case, you and your sibling will have a better than 50-50 match.)
These percentages represent two different levels of "filter."


text:
How do anaerobic bacteria produce ATP for their own cellular activities?
Anaerobic bacteria utilise glycolysis:
Glucose + 2 P + 2 NAD+ => 2 ATP + 2 H + 2 NADH + 2 H2O + 2 Pyruvate
followed by fermentation:
Pyruvate + NADH => Lactate + NAD+
The resultant NAD+ formed can then be used again to break down more glucose molecules in glycolysis to produce ATP.
However, besides NAD+, glycolysis also requires an input of 2 ATP at the beginning (for the phosphorylation of glucose to glucose 6P, and fructose 6P to fructose 1,6 BP)
Since only 2 ATP is produced from glycolysis initially, would these 2 ATP be reused in another round of glycolysis?
If so, how do anaerobic bacteria produce a net amount of ATP for cell activities and growth?

Please go back and check your sums and re-read the chapter in your text book, taking particular account of the fact that two molecules of triose are produced from one hexose.

That was already accounted for in the balanced equation above. 4 ATP - 2 ATP invested is a net of 2 ATP from glycolysis.

What do you mean by "reused"? The net gain of the fermentative type of anaerobic energy extraction from glucose is 2ATP---which is available for cellular processes that need ATP to proceed. Note, that there are two ways to regenerate NAD+: fermentation (which you mention) and anaerobic respiration (which you do not mention); the net gain of anaerobic energy extraction from glucose involving anaerobic respiration is 2ATP & 2NADH, because the latter can be used to generate ATP (via ATP synthase).

Your response to my comment is incorrect. As I said, please go back to your text book and look at the pathway of glycolysis and the actual reactions where ATP is generated and whether the substrate is triose or hexose and if it is triose how many trioses came from the original hexose.

@user1136 — The equation given by OP is not quite right. It lacks ADP and appears to involve phosphorus and molecular hydrogen. If the OP recognized that there was a net yield of 2ATP he would have included 2ATP on the left-hand side of the equation and 4ATP on the right. Indeed, if he had recognized there was a net yield of ATP he would not have entitled his question as he has. He obviously thinks there is no net yield because he has forgotten to multiply by 2 after aldolase. Perhaps that's why he has kept a low profile in the month since he posted. He may even have taken my original advice.

@user1136 NAD+ is regenerated in the NAD+ regeneration reaction that follows glycolysis in which the pyruvate products of glycolysis breaks down into lactate or alcohol depending on which organism you are talking about.

@user1136 you asked how NAD+ regenerates.

The product is 4 ATP not 2, 2 is the net product because two are used to start the reaction.
Looking at the complete glycolysis reaction helps.

ATP can be used to start another round of glycolysis which yields 4 ATP which can then start 2 rounds of glycolysis which yields 8 ATP, rinse, repeat. It is an exponential process, ATP can be taken from this for other processes since as long as you still have 2ATP around to can restart the exponential cascade. For example from the yielded 8 if you take half for other uses, you still get 8 ATP from the next round of glycolysis reactions.

During the reactions, the resultant molecules are dispersed in the cytosol, and it is a bulk phenomenon rather discrete and independent event. The calculations are mainly based on in vitro experiments, so the reuse of the energy transporter molecules (ATP), totally depend on it's quick availability.
The NET production of ATP cannot be determined in precised manner as pathways may show reuse of the formed energy bags (ATPs) or may use already present molecule or molecules from some other reaction.

@VishalKumarSahu Can you please provide some references to support your answer?

There is a lot of theory and scientific articles available through google. If this is a scientific (not for general people) forum, please let me know, I would not use researchgate, pubmed...

Anaerobic respiration, which is used by some Bacteria and some Archaea, is not glycolysis+fermentation. Anaerobic respiration is like aerobic respiration which includes ETC (electron transport chain). Basic difference is the terminal electron acceptor. In aerobic respiration the terminal electron acceptor is oxygen. On anaerobic respiration the terminal electron acceptors are various materials, for example hydrogen sulfide. Read this or research similar sources.
In Turkey, we were teaching anaerobic respiration and fermentation as the same things in high school biology lesson until a couple of years ago. May be you are asking in this regard. If so, rename your question.

source: Stack Exchange

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

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text:
What kind of mushroom is this, and is it edible?

I found these growing on the side of some trees (mostly birch) in my local forest in Gothenburg, Sweden, and was wondering if you could help me with identifying them.
I think they smell of aniseed however my wife thinks they smell of farm animals!
The spore-trace turned out white, if that aids with identification.

Might be oyster mushrooms; look them up. Generally one learns to identify some edible mushrooms and then looks for them. Picking mushrooms and then trying to determine if they are edible is not recommended.

Thanks for the help blacksmith37. Just out of curiosity, why is that not recommended? And by whom is it not recommended? I've always found it more helpful to learn identification with a specimen at hand.

I have several "mushroom" guides , don't remember which ones said it. Pick and examine them with the prospect that the same species may come back in the same spot when you are very familiar with them.

Thanks blacksmith37, I shall keep that in mind. The spore-trace turned out white, so I think you may be right in calling the oyster mushroom.

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


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What is the difference between phyletic and phenotypic gradualism?
As I understand it, Phenotypic gradualism describes the development of new traits as a series of incremental steps.  How is Phyletic gradualism different?

By "phenotypic gradualism", did you mean "phyletic gradualism"?

I will assume that by "phenotypic gradualism", you actually meant "phyletic gradualism".
Phyletic simply refers to evolution of a lineage. It is relatively rarely used term. phyletic gradualism comes in opposition to punctuated equilibrium. Punctuated equilibrium is the notion that a lot of evolutionary change in a lineage takes place over short periods of time interspaced by period of time where very little evolutionary change happen. Gradualism is the notion that evolutionary changes happen very uniformly over time. For more information have a look at evo101 > More on punctuated equilibrium

Actually my text, Zoology by Hickman, Robertson et al, differentiates between Phenotypic gradualism and Phyletic gradualism, hence my question.

Can you please give a direct quote that talks about the difference between these two concepts. That might help


text:
Do oysters feel pain?
Do oysters feel pain when you bite into the inside, or when you crack open the shell? I tried google searching it to no avail. When you bite inside the oyster or when you break the shell to open the oyster, does it feel pain?
EDIT: (Since some people think that mine is a duplicate) I'm asking if the oysters feel pain when we eat the inside, or when we crack open their shell. To the least of my knowledge, ants and oysters have a different body so I don't know if they do feel pain.

Possible duplicate of Do ants feel pain?

This question is already answered by many of the "do X feel pain?" questions.

This is not duplicate of 'Ants feeling pain' since ants and oysters have different organisation and differ in terms of their sensory organs.

@VishalKumarSahu no, but a lot of those questions need to start with definition of pain. We can't measure "pain" of an organism, only observe reaction. So OP can google more about oysters and how they react to X

You should define what you mean by "pain". Do you mean "pain" simply as a reaction causing them to do something such as (try to) withdraw from the cause of the stimuli, and possibly ability to develop automatic reactions to similar situations so they try to avoid the experience of this pain in future? Or do you mean something deeper, "suffering" or "psychological trauma" or "fear of pain"?

I saw a text across the internet (antivegan joke) claiming even plants feel pain. Even when they are already cut. I'm just wondering what is your intention? To claim that oysters should not be ate? Any being tries to survive, whether it feels pain or not and you eating them already contradict their "goals".

I just wanted to know whether they feel pain so maybe I can eat them quicker and make their death quick. It does sound a little.. weird.. but I do like eating oysters.

I vote to transfer this question because it is about philosophy, not biology.

There are fundamental problems with defining what it means for an animal to feel pain, especially when the animal is a life form as different from us as an oyster.
I wasn't able to find any specific info online about oysters, but there is quite a bit of information that allows us to reason by analogy with related species.
Oysters are molluscs, and molluscs do have brains and sensory systems, but their level of sophistication varies a lot. Cephalopod molluscs, such as squid, octopuses, and cuttlefish, have extremely sophisticated nervous systems, and it has been argued (Peter Godfrey-Smith, Other minds, 2016), that we should think of intelligence as having arisen twice on earth through parallel evolution: once in vertebrates and once in the cephalopods. Cephalopods have sophisticated communication systems, and they can use tools and solve problems. There has been extensive research on pain in cephalopods.
So it's inherently pretty plausible that cephalopods can (in some difficult to define sense) suffer and feel pain, and by extension that their less advanced cousins the oysters can as well. However, the nervous system of an oyster is much more rudimentary than that of a cephalopod. A better analogy might be with snails, and there is some research on snails. They avoid damaging stimuli, have opioid systems, and respond to morphine and naloxone analogously to humans (e.g., showing less aversion to a hot plate when they've been dosed with morphine). So it seems likely to me that oysters can feel pain (for some reasonable definition of the word), but this whole area is one where people don't really know the answers to the questions or how to construct the philosophical foundations.

It’s already implicit in the answer, but I think it would be clearer if you made explicit the distinction you are (seem to be?) making between pain and suffering, namely that pain is the physical activation of appropriate neurons that results in avoidance behavior, and suffering is the psychological experience of being in pain and the stress and, for lack of a better word, unhappiness that causes. Oysters (and most mobile animals) clearly seem to have the former (and so might some plants, and other life forms), but the latter is a much, much harder question to answer.

It is very unlikely that oysters feel pain however it's not clear what the question actually means
What does it mean to say something feels pain? The most reductive biological interpretation is to say that "feeling pain" is simply the capacity to sense damage, or the threat of damage, to the body and communicate that to the nervous system in a way that elicits a response. However, that's not really what we're usually talking about feeling pain, but rather the unpleasant sensation that accompanies these signals.
And that's more difficult, because we know that the two are not equivalent. For example, disabled athletes are able to improve performance by inflicting injuries they cannot directly feel, but their bodies still respond to. In this case the reductive biological pathways are active but the sensation of pain is absent.
Oysters have no brain, but simply an couple of enlarged ganglia that perform some rudimentary centralised functions, and so it seems very unlikely indeed that they are capable of experiencing any sensations and thus almost certainly do not experience pain in the sense we would usually use of "feeling pain". But they do have a nervous system which can respond to stimuli including damage, or threat of damage, to their tissues so they have what could be described as having a pain response.

I agree with you that there are fundamental problems of definition here. But since I reach an opposite (tentative) conclusion to yours in my answer, I'm curious what you would take exception to in my answer. Does the evidence I give about snails not convince you that snails feel pain?

@BenCrowell: No, it doesn't; it convinces me that snails have a pain avoidance response. I do not think that this is either equivalent to or implies that the snails feel a sensation of pain.

Referring to this research article on PubMed, oysters have their sensory system and organisation like humans. So any change or invasion in the system of Oyster is communicated through sensory organs. So Oysters do feel pain. It's like, pain is a result of something harmful or negative is going on.
Regarding break opening the shell, as it is a sort of insult to their protective system, they have the sense of removal of the covering, we can term it as 'pain'.

Articles listed on PubMed are not necessarily from NIH, any more than websites you find through a Google search are not from Alphabet. All the paper you mention demonstrates is that oysters have a nervous system, which is far from controversial and says nothing about the organization of their nervous system with respect to humans. From a neuroscientific perspective, pain and sensation are not the same; I suppose yes, you can term it 'pain', but I could also hold up an apple and term it 'pain': that doesn't mean it's valid or is how people in the field talk about pain.

"they have the sense of removal of the covering" I would be very interested in how we would prove/disprove such a statement.

@BryanKrause, but an apple is not a sensation. And this is not meaningless, how can you know other people feel pain and not just a sensation? Monkeys, fish, worms?

@rus9384 Other people, as well as monkeys, have the exact same neural organization of pain pathways. Fish have some similarities, though not identical; worms are much different. It is quite possible in humans to have reflexes without pain, and other types of sensation are carried separately from painful ones, so simply having sensation does not mean having pain, even in the context of aversive stimuli. That also doesn't prove that something like an oyster doesn't have pain, but if it does it is instantiated differently than ours. The answer says "oysters feel pain" without support.

Please add options for the questioner, about the education like if he is graduate or post graduate, if he has published paper or not, and the people who give answer should answer based on that. or always answer like they do publish a research paper.


text:
Error frequency of DNA replication without proof reading activity of DNA polymerase?
Different domains of DNA polymerase contain different activity, like 5'->3' polymerisation and 3'->5' proof reading activity (a general case), and these domains can be exploited separately to make them perform single activity at a time. For example if we are conducting detection of some sort of mutation on a strand of DNA, we need to suppress the activity of DNA polymerase proof reading, ie, stopping it to correct the error it makes.
Since the proof reading activity increases the fidelity of replication to some 99.9%, I want to know what would be the efficiency if there is no proof reading activity.
To simplify my question-
If DNA repair system commits 1 mistakes out of 10^8 base pairs it added in nucleotide chain, how many errors would occur if we remove it's proof reading mechanism?

What research have you done to find the answer to this question yourself? Have you looked at related questions on this list? Try the right-hand side bar. There were questions recently on this topic and you will find the answer there.

Actually I don't understand the dna sequencing tag

@David do I need to show you my research papers or my notes to be able to ask question here?

@Shred DNA sequencing tag is for those people who mostly use DNA exonucleases for sequencing which is also related to my question.

The objective of this site is "to build a library of detailed answers to every question about biology". So, obviously, the first thing you should do is check that there isn't already an answer to your question here. The Help to this site provides tips on asking good questions, in particular : "Have you thoroughly searched for an answer before asking your question? … This demonstrates that you’ve taken the time to try to help yourself, it saves us from reiterating obvious answers."

Instead of falling in any ambiguity I should stop being here as I thought that I can have discussion beyond what I read through books. As books don't have hypothetical or very current ideas.

Klenow Fragment could be used to have a polymerase which lacks the exonuclease activity: not just the 5' -> 3' but also the 3' -> 5' .
Lacking the exonucleases activity, the only kind of control is given by the biochemical property of the enzyme: remember that the DNA polymerase has an active site similar to a right hand, which make possible to have correct couple between A,G,C,T. Then, according to this study, the error rate is something around 1e-4.


text:
How does vasoconstriction retain heat?
I am reading on vasoconstriction on wikipedia. The article states that:

When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance.

Why/How exactly is the heat retained when blood flow is decreased? Isn't it the case that when things slow down they generally get colder?

Did you read the next sentence after the one you quoted?  It says "This makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat."

@mgkrebbs I did read that, but I thought it was an extra reason and somewhat distinct from the quote. The part "thus retaining body heat" implied that the reason was already mentioned and this is just the consequence.

Think of the body as a heat-sink. We can let off heat by using our fluid exchanges – namely, blood and sweat. When we exercise, sweat cools us off through evaporative cooling. When we’re not exercising or in warm weather, we’re generally not sweating, but we’re still exchanging heat with our surroundings – after all, the metabolism is still active, we’re still “burning energy,” and our skin never reaches air temperature nor does our core cool to the temperature of our skin (so some kind of heat exchange has to be happening). How can that be, when there’s no obvious mechanism to carry away our heat as in the case of sweating?
The answer to this lies at the heart of your question. Human thermoregulation is largely thanks to our blood flow and vasodilation:

“Skin blood flow in adult human thermoregulation: how it works, when it does not, and why.” Charkoudian. N. Mayo Clin Proc. 2003.
Cutaneous sympathetic vasoconstrictor and vasodilator systems also participate in baroreflex control of blood pressure; this is particularly important during heat stress, when such a large percentage of cardiac output is directed to the skin. Local thermal control of cutaneous blood vessels also contributes importantly—local warming of the skin can cause maximal vasodilation in healthy humans and includes roles for both local sensory nerves and nitric oxide. Local cooling of the skin can decrease skin blood flow to minimal levels.

In essence, your core “wants” to stay warm. If the air around your skin is comparatively warmer, cutaneous blood vessels will dilate to accommodate a higher flowrate, allowing more blood to engage in heat transfer. The opposite is true for air that is comparatively colder, and the relationships between cutaneous blood flow, sweating, and local skin cooling can be tested experimentally:

“Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans.” Wingo et al. J Appl Physiol. 2010.
In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.


text:
Is there logic in this sentence? "Authors discovered a gene as one of the genes evolved through natural selection"
From a news report:

PhD candidate Daiki Sato and Professor Masakado Kawata have discovered SLC18A1 (VMAT1), which encodes vesicular monoamine transporter 1, as one of the genes evolved through natural selection in the human lineage.

Didn't all genes evolve through natural selection?
I'm self-training myself in translation into Russian, and this sentence stumped me. How do I translate it and avoid an absurdity? I thought that all genes have evolved. That's what genetics is about, isn't it?

I think if you can read that sentence a bit differently and then it makes much more sense: if you put (more) emphasis on the last part [natural selection in the human lineage] it becomes clear that in this case we are talking about natural selection (or like iayrok clarified in his answer, positive selection) respective to the evolution of humans. And here obliviously not all genes are equally affected since, we share a lot with out animal ancestors.

Yes, the statement in the news article is not correct; however, it (probably accidentally) isn't quite as nonsensical as it sounds.
The actual paper that the news article is trying to describe is unsurprisingly more accurate.

Here, we found a gene, SLC18A1 (VMAT1: Vesicular monoamine transporter 1), as a positively selected gene in the human lineage. This gene has a human‐unique variant (Thr136Ile; different from other mammals (136Asn)) whose association with several psychotic symptoms has been repeatedly indicated. Moreover, our analysis showed that this variant has been maintained in non‐African populations by balancing selection and had originated around 100,000 years ago, typically regarded as the timing of Out‐of‐Africa migration.

--Positive and balancing selection on SLC18A1 gene associated with psychiatric disorders and human‐unique personality traits
Here instead of talking about "natural selection", the authors refer to "positive selection" and "balancing selection", two sub-categories of natural selection. Since much of the genome is under negative selection, it's worth noting alleles that are not.

Didn't all genes evolve through natural selection?

The reason the news article is not nonsensical is that natural selection is not the only force that acts on genomes.  We've known for 50 years that drift is an important factor that influences genetic evolution (wikipedia: Neutral theory of molecular evolution, Nearly neutral theory of molecular evolution).  However, it's pretty clear from the article that the author is unaware of these concepts and probably doesn't understand the significance of the paper.

Every time I see how badly journalists misunderstand the scientific news they report on, I wonder how accurate is their understanding of, e.g., the political news they report on.

@DavidRicherby "Gell-Mann amnesia"


text:
are more males born than females?
I believe that given what I have heard about war and that up until whenever only men fought in wars then to replace the amount dead so that it would be equal on earth then more male births would occur than females. what is your thought?

Yes, the ratio is around 1.07:1, for males to females. But this is likely due to far more factors than male mortality rates. Also, it would've been quicker to Google your question than to ask Stackexchange.

Your post is mainly constituted of a single large sentence. This sentence is very hard to understand and is full of grammatical issues (you might be an ESL, like I am myself). That makes it hard to understand your question. Also, please capitalize the first letter of your sentences.

Are more males born than females in humans?
According to the CIA (the only reference I could find; see here click on "people and society" and look for "sex ratio"), the world wide sex ratio at birth is 1.03 males for every female. This sex ratio is reversed at old age (women's life expectancy is higher than men's).

at birth: 1.03 male(s)/female
0-14 years: 1.07 male(s)/female
15-24 years: 1.07 male(s)/female
25-54 years: 1.02 male(s)/female
55-64 years: 0.95 male(s)/female
65 years and over: 0.81 male(s)/female
total population: 1.02 male(s)/female (2017 est.)

Note that these statistics somehow ignores the cases of intersex which accounts for a not completely negligible part of the population (see here). In short, yes, more males are born than females.
Why are there more males born than females in humans?
It is unclear from your post whether you are looking for proximal or ultimate causation and your explanation is made unclear by the bad grammar in your post.
Orzack et al. (2015) (thanks @iayork for the reference) investigate the reasons for this unequal sex ratio at birth. From their abstract

Our results indicate that the sex ratio at conception is unbiased, the proportion of males increases during the first trimester, and total female mortality during pregnancy exceeds total male mortality

While I have not read the whole paper, intuitively, I would tend to think that females babies might have a higher miscarriage probability, which cause the observed discrepancy. For example, X chromosome inactivation (dosage compensation) that happen in females only, and the development of female reproductive system (which is arguably more complex than the male's reproductive system) could cause of higher miscarriage probability among females than males. This is all hypothetical though and you should have a look at the link paper.

I don't know of any study that investigate the reasons for this unequal sex ratio at birth. There are many. A recent review (The human sex ratio from conception to birth) concludes that "total female mortality during pregnancy exceeds total male mortality".

This is a big correction of my post and an important add up (you could have made it a new post). Thanks. I edited my post.


text:
Is too much CO2 in the air toxic?
I know that if there is too much CO2 in the air we will have too much greenhouse effect.
I would like to know if there is too much CO2 in the room, something like 3% while there is also more that adequate oxygen for us to breath. will we live or die? why?

CO2 forms carbonic acid in water, which helps to dissolve rocks and mountains in envitonmental science. It would slightly acidify your body with what is called a weak acid.
5% can cause acidosis and loss of conciousness, without lack of oxygen.
3% would devastate most chalk based sealife, corals and shells.
Perhaps lifelong breathing of 3% co2 would have serious effect on alkaline processes in the body, osteoporosis, and would have to be counterbalanced by the body to maintain its blood ph above 7.35, with alkaline chemicals like sodium.
Also check out this fact sheet.

First, the toxicity of any  substance is a matter of dose. So the answer of your question is yes too much is toxic but the real question is how much is too much ?
This is still not clear in the litterature but effect are starting to appear over 3% see:
HAYWOOD C., BLOETE M.E. -
Respiratory responses of healthy young women to carbon dioxide inhalation. Journal of Applied Physiology, 1969, 27, pp. 32-35.
OR
ALEXANDER J.K.,WEST J.R.,WOOD J.A., RICHARD D.W. - Analysis of the res- piratory response to carbon dioxide inhalation in varying clinical states of hypercapnia, anoxia and acide-base derangement. Journal of Clinical Investigation, 1995, 34, pp. 511-532.
CO2 is the result of respiration as you know and a too high concentration in the blood result in a change a Ph of your blood and asphyxia. You can find more information on those effect here Permentier and al.
Hope this helps !

nice answer. You can add more information about physiological impact on hem, but it is still good :).

I know CO2 is toxic if it's too much in the blood. by question can somehow be reduced to how doe increasing the CO2 level of air increases the CO2 level of blood.


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What is the name of this brown fly?
They started mating each other and there are lots of them in our hous. I saw them attached together from their bottom.

They have 6 legs and 2 antennae. They have brown wings. i live in iran, tehran. they are about size of fingertip (or smaller)

Welcomo to Biology SE. I know you are veteran from S overflow, but you should take a look how you should ask at first place. You know, ID questions can be really well  accept but you have to add some information, which somebody can start with. Like, where did you see those bugs, parametr of it and you might get answer. Anyway good luck and enjoy your time on Biology SE.

Thanks for the reply. I saw them in my house. I think they have 6 legs. I dont really know anything about flies. I was just wondering what species are these. Also they fly like a butterfly.

They have solid brown wings

Please edit the question to include the details in your comments. You should also note your location as different countries have different species.

@Michael_A Ive tried to provide information as much as i could.

They look more like moths than flies.


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Determine planar phyllotaxis characteristics
Is there any method to fast and precise count the number of spiral and the divergence angle on a planar phyllotaxis pattern?

The example of spiral phyllotactic arrangement of emerging flowers on Gerbera hybrida. (doi: 10.1093/jxb/erw489)
I'm looking for a method for characterizing any phyllotaxis pattern.

I've found a following protocol for counting spirals on sunflower heads: http://www.turingsunflowers.com/media/Resources/count/Measure_and_count.pdf


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What does 'half life' of a protein mean?
Why do we use the term 'half life' for proteins?
Here is a link to some information regarding this question, but I am unable to infer it.

"Half-life time" is a general term. This is a time after which the amount of substance X decreases by 50%.
If you take a bulk of something (say, 100 protein molecules), if this protein has half-life time of 1 hr, then 1 hr later you'll have 50 molecules left.
In cellular biology it usually means that 50% of protein got recycled/degraded in given half-life time

why is not the term "life time" used?

@souravthampan comparing to https://en.wikipedia.org/wiki/Fluorescence-lifetime_imaging_microscopy I think main difference is that "lifetime" is a characteristic of process, which can be measured by "half life" time.


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What is the function of Xylem parenchyma?
why xylem need parenchyma cells ihave read these cells are connected with xylem by plasmodesma i know that plasmodesma is to connect between cytoplasm of two cells and xylem is dead so what is the need of xylem parenchyma ?

I would like to aswer your question. First definition, function is from this web:

The xylem parenchyma is comprised of parenchyma cells. Parenchyma cells are the only living cells in the xylem. They have thin cell walls, large vacuoles, prominent nucleus, and protoplasts. They have differing shapes although they are usually cylindrical and lobed in form. In the trunks of woody plants, the xylem parenchyma cells are colourless and are believed to be involved chiefly in storing starch, oils, and other ergastic substances. The inclusions in xylem parenchyma cells may contain tanninferous compounds.

And from this article:

Xylem parenchyma cells in contact with xylem conduits are assumed to simultaneously generate the energy gradient (deposition of solutes in the form of sugars, ions or a combination of both) that allows water to flow into empty vessels/tracheids, and supply water for refilling (Zwieniecki & Holbrook, 2009). Regarding the first task, the initial research focus has been on finding the source of osmoticum through analysis of carbohydrates in the parenchyma cells and the role of phloem in the delivery of sugars to sustain refilling. Both enzymatic analysis and visualization techniques have demonstrated that starch levels in living parenchyma cells adjacent to xylem vessels decrease on a timescale coincident with embolism refilling (Bucci et al., 2003, Nardini et al., 2011a, Sakr et al., 2003, Salleo et al., 2009, Secchi & Zwieniecki, 2011).


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Self Grown Organs
Could a viable organ be partially grown in a test tube then be hooked up to the host in some way until it is large enough to swap it with the bad organ?
For example: Could a smaller replacement heart have a tiny pacemaker to keep a separate heart rhythm and grown in a different part of the body cavity like the appendix?
Then when the organ is mature, remove the organ from the appendix and then transplant to another person or on oneself?

Speculative questions like this are not good for Biology.SE; unfortunately, because of the bounty I cannot currently vote to close.

I don't understand your comment.

@BryanKrause I noticed that you have to wait 2 days before a bounty can be placed. If a question goes unnoticed it could be locked in by a bounty. If the time limit is extended the bad question could be closed with less rush.

I don't think questions are closed with rush, they should be closed quickly, and also it is important to note that questions that are voted to be closed are initially put on hold; they have several days to be improved and brought back if the improvements solve the problems that led to close votes. However, this is a discussion for Meta.

While the specific hypothesis on potential implementation (given as example) is very speculative, it is not needed to answer the core question.

Could a viable organ be partially grown in a test tube then be hooked up to the host in some way until it is large enough to swap it with the bad organ?

Yes. This conceptual possibility already is a reality for one organ, namely the skin.
For an example see the following story in a good scientific journal: https://www.sciencemag.org/news/2017/11/boy-rare-disease-gets-new-skin-thanks-gene-corrected-stem-cells
Unfortunately this doesn’t yet mean that conceptually homologous procedures could already be performed for most organs.


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Worm in water identification help
I live in Auckland New Zealand. I have been growing Chia seeds in bowls with just water. I noticed after a couple of weeks, these white / transparent worms appeared in the bowl. It seemed that they came out of nowhere? I have seen them crawling in my bathroom before. And the really big ones can get up to a 2-3 cm, so they can't possibly be drain fly larvae as they can grow to a few cm? I also did not see any drain flies nearby. I wonder what type of worm are they? I hope they don't come from tape water, because I have been drinking from it directly.

[EDIT] - Photo of the worm in bigger size (~1.5cm):

Are you sure they're worms? They look like sprouts, either roots or stems.

They look like mosquito larvae, but it is quite hard to be sure: They are so tiny.

Agree with @Astrolamb they are sprout of green grams

@Astrolamb They are moving around!

@bli They are tiny now - but they are growing. I have seen 3cm big ones.

@Astrolamb Yes there are stems and roots in the photo. The other smaller ones are the worms. They are moving and crawling in the water. They can crawl out of water as well. Amphibious?

@JerryH Try to add photos of the larger ones.

@bli - 1.5cm one

In the end, I don't think this looks like a mosquito larva.

They won't be from the tap water, unless you have had something lay eggs in the tap nozzle itself; NZ has high standards of water quality for municipal water and tap water is safe to drink throughout NZ.


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Help identifying a fly by its remains
I recently hiked in a swampy forest in the Yaroslavl region(Eastern Europe) near lake Plesheevo and came across a clearing. Although the area was swampy and verdant, there was a 5 meter wide "bald spot" on the ground which looked like sand. Near that spot there was a lot of buzzing (which I initially mistook for the buzzing of wasps), and soon I found myself covered in these black flies.
The flies clung to my fabric hoodie, at least one tried crawling in my hair, and one tried to find its way into my eye.
I tried shaking them off, but they seemed to be able to cling very firmly to my clothes. (later I discovered that even dead flies were really hard to remove from fabric)
At that point I panicked, quickly retreated, and spent a good 15 minutes extracting every single one of them from myself and my garb.
When I came back, I took a picture of the carcasses of two flies that found their way into my pocket and silently passed away there from unknown causes. Unfortunately, I didn't get to take a picture of a living fly because I was too agitated at the time.

Their length was approximately 0.3 inches and when squashed, they produced yellow spots on my clothes.
I tried identifying them, but didn't have much success. They seem to look like a variety of horse-fly (or a dear-fly), but I think none of them actually bit me. Also, strangely enough, my clothes were sprayed with insect repellent which they seemed to either completely ignore or were actually attracted by.

They look very much like Hippoboscidae. https://en.wikipedia.org/wiki/Hippoboscidae
This family are parasites of birds and mammals, but I am not aware that they are vectors of any diseases to humans. So don't worry. One member of the family is a wingless parasite on sheep (Melophagus ovinus)

Thanks, I think that's it! It seems I was "assaulted" by a spawn of deer flies (for some reason Wikipedia has 2 articles on deer fly, and the one I initially linked was not "the right one"?) The article mentions their bodies are hard to remove once they've attached themselves to the victim (check), they prefer dampness (check), they reproduce on moose and deer (which are numerous in that area), and it can be found in the European part of Russia (check).

The Russian Wikipedia entry also mentions the deer flies can transmit the Lyme disease to humans, albeit somewhat rarily. So it seems to make sense to get checked if bitten after all.

These were NOT deer flies (Tabanidae). That is the problem with common names, that differ across languages. They may have been Deer keds, which are in the family Hippoboscidae.

Interesting, the English Wikipedia page lists both of these names as synonymous for Lipoptena cervi. I guess they're only synonymous in some people's vernacular.

Common names are often used for different species, even in any particular language. The people using the common name are simply not distinguishing the differences, even when organisms given the common name are quite different.


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Misuse of DNA leaks to create your clones, or children
Recently, sequenced DNA data leaks have been reported.
The linked article discusses possible risks like blackmailing based on health related data.
However there could be one more misuse, at least theoretically, therefore this question. For not specialists, actually good to know.
Is it by current state of the art technically possible using this DNA data to (given you have fully sequenced DNA of an individuum):

clone this individuum?
engineer artificial gametes to breed his/her children?

I voted to close because this is science fiction, not present-day science, which should answer your question: We are not remotely close to being able to do what you suggest.

I don't understand, why this question gets down and close votes for basically asking "Is this science or fiction?"

As @iayork mentions in their comment, creating a human clone from a sequenced genome is still in the realm of science fiction. Also, DNA testing companies like MyHeritage don't sequence the client's entire genome. They typically analyze the client's DNA with a SNP Chip that compares the client's DNA to known reference sequences at several thousand position with well known variations in the human population.


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What kind of spider is this? I have never seen one like this before

This was on my butterfly bush yesterday with a moth by the neck.  I have never seen one like this before.  Just wondering what the name is.  This is in southern Illinois.

Excellent picture!  Someone will know this -- might take a day or two.

On iNaturalist I found a very similar picture, of a White-Banded Crab Spider.  It is found in your area.  It's a possibility.


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Flow diversion for cerebral aneurysms or stabilizing the hemodynamics?
I'm doing research of flow diverter for cerebral aneurysms applications and I'm wondering the reason behind stent placement underneath of cerebral aneurysms is to divert the flow or stabilize the hemodynamics (e.g. reduce wall shear stress or blood flow velocity in the aneurysmal region)? Let's say people do it to divert the flow and prevent blood to enter the aneurysmal region. That looks fine for side wall aneurysms when there is no smaller arterioles or branches connected to the aneurysm, but for terminal aneurysm where the flow diverter may block the blood flow into smaller arterioles, is it a appropriate case to deploy stent? I mean if we prevent the blood to enter some part of smaller arterioles how brain could maintain its functionality due to its need for oxygen. I appreciate if someone could explain the logic behind the flow diverter placement in the cerebral aneurysms.

I don't quite understand the dichotomy you present between diverting flow and stabilizing hemodynamics. The former is a direct outcome and the latter is a secondary outcome: both are goals.
The overall goal is to isolate the blood in the aneurysm and allow it to clot and heal over time. Embolic coils are also used to assist the process, in which case the flow diverter helps to keep the coil in place and the resulting embolism out of the primary circulation.
One would not typically deploy a flow diverter over branches that one wishes to remain patent, although patency can be maintained in smaller vessels. In many neurovascular situations, collateral circulation can make it acceptable to occlude a branch, however.
You may be confusing plain stents with flow diverters; a plain stent has as few struts as possible while maintaining structural support (though high flow through the struts can cause turbulence and is something you want to avoid if possible), and creative stent placement techniques including deployment of multiple stents and use of balloons to break open strut configurations can be used. These do not block flow per se, but can help keep coils in place and maintain the desired structure of the vessels involved.
I've included several references that I quickly gathered; these may not be the most ideal references but should give you a look at some of the approaches used. I would strongly suggest you look through the rest of the literature using search terms from your question to get an idea of how interventionalists approach different situations.
I'll add that I am not a physician and am not up-to-date with the latest guidelines or standard of care, but in my experience with the literature a lot of these decisions are up to the experience of the physicians involved and based on a lot of case study; randomized trials aren't really possible to cover all the anatomical variety that is experienced.

Burkhardt, J. K., Riina, H. A., Tanweer, O., Shirani, P., Raz, E., Shapiro, M., & Nelson, P. K. (2018). Flow diversion and microvascular plug occlusion for the treatment of a complex unruptured basilar/superior cerebellar artery aneurysm: case report. Journal of neurosurgery, 1-6.
Chow, M. M., Woo, H. H., Masaryk, T. J., & Rasmussen, P. A. (2004). A novel endovascular treatment of a wide-necked basilar apex aneurysm by using a Y-configuration, double-stent technique. American Journal of Neuroradiology, 25(3), 509-512.
Miyachi, S., Matsubara, N., Izumi, T., Asai, T., Yamanouchi, T., Ota, K., ... & Wakabayashi, T. (2013). Stent/balloon combination assist technique for wide-necked basilar terminal aneurysms. Interventional Neuroradiology, 19(3), 299-305.
Puffer, R. C., Kallmes, D. F., Cloft, H. J., & Lanzino, G. (2012). Patency of the ophthalmic artery after flow diversion treatment of paraclinoid aneurysms. Journal of neurosurgery, 116(4), 892-896.
Siddiqui, M. A., Bhattacharya, J. J., Lindsay, K. W., & Jenkins, S. (2009). Horizontal stent-assisted coil embolisation of wide-necked intracranial aneurysms with the Enterprise stent—a case series with early angiographic follow-up. Neuroradiology, 51(6), 411-418.
Wong, G. K., Kwan, M. C., Ng, R. Y., Simon, C. H., & Poon, W. S. (2011). Flow diverters for treatment of intracranial aneurysms: current status and ongoing clinical trials. Journal of Clinical Neuroscience, 18(6), 737-740.

The flow diverter and plain stents are used interchangeably by authors, whom do not have any medical experience and are engineers like me, in the literature. At least is there any way to find out in which case we need to put plain stent or flow diverter?! Also, is it possible to explain a little bit more about plain stents and its application and what does it do to change hemodynamics? I appreciate your help.

A plain stent has no covering on it, it's just metal mesh. It provides structural support and keeps an embolic coil inside the aneurysm. If you are engineers and have no medical experience, you should really find an interventional radiologist/neurosurgeon/whoever does intracranial embolism at your institution to discuss with. I'm neither an engineer nor a physician but I did have a job bridging exactly that gap for engineers in the area of intravascular devices; the engineers often didn't even know what they didn't know when they came to us and talked a lot about how much they benefited.

Ok you made the question more interesting to me! What is that cover you are talking about in the flow diverters? it's a coating? If yes, do you know what's the material of that coating and its purpose perhaps? I mean I really apologize to ask a lot of question from you. But I believe you are the only person here which knows these kind of things. I really appreciate your help!

Yes this is a small community, I doubt you will find another person here who did R&D with stents. I think I am partly mistaken about the flow diverters, as I was thinking these are covered stents but it seems they are just high-metal density stents. They just have more struts for a given area and are meant to occlude to some extent, whereas normal stents are meant to avoid occulsion as much as possible (i.e., to provide as much support as possible with minimal contact to tissue). I'll make sure to update my answer.

One interesting question about occlusion is that: a lot of researches in the literature claim that low wall shear stress is responsible for cerebral aneurysms' rupture but when we put flow diverter (FD) it will reduce the wall shear stress in the aneurysmal region because it prevents the blood to enter the aneurysm. So, does it increase the rupture risk or decrease it? I mean in the literature people are saying FDs reduce the wall shear stress and that will help to occlude the aneurysm but if the low wall shear stress is responsible for rupture, it looks counter intuitive to me.

I'm not an expert in aneurysm biology but my suspicion is it isn't low wall shear stress per se, but rather that the vascular wall in the area of the aneurysm thins where wall shear stress is low, leading to rupture risk. In the case of aneurysm treatment, the goal is to clot up the aneurysm space and have it heal, and that this should happen faster than the wall integrity would decay. That said, I also would expect that intervention would create a brief period of higher risk for rupture; that risk must be accepted to prevent longer term risk.

I really appreciate your help! Do you have any reference or keywords for these low wall shear stress things and maybe higher risk of rupture after intervention for a brief period of time? Thank you so much! You cleared a lot of things to me!

Search google scholar for "low wall shear stress aneurysm": first result I get is Boussel, L., Rayz, V., McCulloch, C., Martin, A., Acevedo-Bolton, G., Lawton, M., ... & Saloner, D. (2008). Aneurysm growth occurs at region of low wall shear stress: patient-specific correlation of hemodynamics and growth in a longitudinal study. Stroke, 39(11), 2997-3002. and seems very relevant. For the latter, I would just search for "complications" after embolic coil/neurovascular stent/etc etc.


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Is Human a race?
Is it correct to say that 'humans' are a race? Will it also include apes and chimpanzees?
Can I use the terms 'species' and 'race' interchangeably?

You should clarify what are your definitions of 'species' and 'race'. It's not clear whether you are asking about biological taxonomy where such category as 'race' doesn't exist, or about human categorization where it's pretty much social construct.

"Race" is a very informal and sloppy term that you would use below the rank of "sub-species", another vague and unrestricted term that I asked about a while ago. Species is much stricter and has some biological/taxonomical meaning.

The term "race" in biology
The term "race" is sometimes used in biology as a level of categorization below the species level. It is hence not a synonym of "species" but closer to a synonym of "subspecies". The term is however quite rarely used to my experience.
The term "race" in the popular literature
In the popular literature, the definition of the term "race" has varied quite a bit through time (see wikipedia > Historical race concepts). It also vary a lot through languages and cultures. For example, in french, the term "race" is generally understood as synonym of "species", while in english it is generally understood as synonym of "ethnic group". Below, I will focus on the english definition.
From wikipedia > race

A race is a grouping of humans based on shared physical or social qualities into categories generally viewed as distinct by society.

Hence, the term "race" (in the 21st century and in english) is often used as synonym of "ethnic group" (see here). Note that ethnic groups are defined very arbitrarily and have been defined much before we started to study the genetic structure of human populations. As a result the standard categorization of humans into ethnic groups only poorly represent the existing genetic diversity. For example, consider the categorization "Sub-saharan Africans, caucasians, Asians, Amerindians, and native Australians" referred to by
@Eff in the comments. In here, the category Sub-saharan Africans, in itself represent the majority of the genetic diversity among humans (I eyeballed this claim from figure 1 from Tishkoff et al. 2009)

It is hard to read the post here. It is a phylogenetic tree of human populations. The below two third of the graph contain only African populations. Hence the non-African populations are nested within the African tree (or in other words, "African" is not monophyletic). See also the post Human genetic diversity in Africa in comparison with the rest of the world. To be clear, I do NOT mean that the classical grouping of populations into ethnic groups does not represent any genetic structure, I only mean that those categorization were made somewhat arbitrarily and hence only poorly reflect the genetic structure of populations.
Keita et al. (2004) is a very good read on the subject.
Questions of interest

Is the concept of species somewhat arbitrary?

Yes, it is somewhat arbitrary. For more information, please have a look at How could humans have interbred with Neanderthals if we're a different species? .

Are there several species of humans or is there only one species of humans?

Have a look at Does it make sense to classify all humans in a single species?

Are there different "subspecies" of humans?

Typically, we do not consider subspecies of humans. However, this decision is somewhat arbitrary. The standard classification of humans into ethnic groups is only a poor representation of the genetic structure in humans. You will note that most of the genetic diversity in humans today is found in Africa only (see the post Human genetic diversity in Africa in comparison with the rest of the world).

Is it correct to say that 'humans' are a race? Will it also include apes and chimpanzees?

Humans are usually considered a species. Other great Apes such as Chimpanzees for example are considered a separate species from humans. Some people consider neanderthals as the same species as humans but different subspecies hence calling neanderthals Homo sapiens neanderthalis instead of only Homo neanderthalis. When considering neaderthals a subspecies of Homo sapiens, we necessarily need to consider humans as a subspecies, then called Homo sapiens sapiens.

Is Human a race?

Humans are generally consider a species (or sometimes a subspecies). The term race, when used in humans is generally used to mean ethnic groups.

Can I use the terms 'species' and 'race' interchangeably?

No, you probably should not. While the term "species" is a somewhat arbitrary concept, it is a concept for which scientist work an agreement based on empirical data. The concept of race on the other hand is often used with very different definition by different people, when used in humans and in english, it poorly represent the genetic structure of populations. Also, the term "race" never really mean "species" to anyone. It either mean something like "subspecies" or something like "some arbitrary grouping" (aka. ethnic group).
On a personal note, I tend to avoid the term "race" as I prefer use the concepts of "ethnic groups" (when dealing with the arbitrary categorization of humans into groups), "subspecies" (when dealing with commonly agreed upon subspecies based on empirical data; there are no commonly agreed upon subspecies in humans), or "species" (when dealing with notion of reproductive isolation) instead so that my interlocutor has a better understanding of what I mean.

Good answer generally, however there are a few things that I think are misleading. "In other words, the standard categorization of humans into races (or ethnic groups) has very little biological basis to it and poorly reflects the reality of population structure." This is false or at least misleading. Self-identified race maps almost perfectly on to genetic clusters as they come out of cluster analysis. If you're talking about the "classic" major races such as Sub-saharan Africans, caucasians, Asians, Amerindians, and native Australians, then genetic clusters fit very well.

While I strongly agree that subspecies has a somewhat arbitrary feel to it, this is just as true for other animals than it is for humans. The reason that humans aren't generally categorized into subspecies while other animals are, is not because of a biological reason. There are many species that have recognized subspecies which have less genetic diversity, less phenotypic diversity, much overlap/continuous variation, etc, and yet have recognized subspecies. It's mostly just not done for humans because it's a socially controversial thing to do to split humans into groups.

@Eff  Thanks for your comments! I tried to clarify what I meant. Please let me know if it sounds correct to you. I have no opinion about your claim There are many species that have recognized subspecies which have less genetic diversity, less phenotypic diversity, much overlap/continuous variation, etc I imagine it is likely true but I do not know a good way to make this comparison (or do not know the literature well enough) to include that in my answer. I'll just leave it with Typically, we do not consider subspecies of humans. However, this decision is somewhat arbitrary.

I think your answer is good, and I agree with most of what you say. I think that species and subspecies are concepts that can be useful, so I don't advocate for never using them, but there is no doubt that they are quite fuzzy concepts (especially subspecies).
When I say that classical racial groupings map well onto genetic clusters, I'm saying that there are many studies that have investigated to which extend there is concordance with self-identified race and best-fit genetic cluster. What you tend to find is that there is near 100% agreement, at least 95%.

@Eff this is not an attack, I am just genuinely interested: is there a citation on hand for these?

@NatWH Sure. There are many studies testing how well best-fit genetic clusters match self-identified racial group. So many, that I won't be able to fit the citations of the individual studies in a comment. Instead, see Neven Sesardic's article Race: a social destruction of a biological concept, where he cites some of the studies testing the accuracy of cluster analysis. If you want just a single example of a study, see e.g. (Bamshad et al, 2003).

@NatWH In the study that I referenced (i.e Bamshad et al, 2003), they test how well the three classic "racial" groups, namely Sub-saharan Africans, Asians, and Europeans, fit genetic clusters (The clusters are made independently without any prior knowledge of where the individuals come from). A quote from the study that I referenced : "When data from all 160 loci were used, the mean correct assignment to the continent of origin increased to 99%–100%."

I'm curious, though: Couldn't you potentially call each node in the above tree - perhaps up to some reasonable limiting depth - a "race", and thus bigger (or "macro") races split into smaller (or "micro") ones, and moreover argue that perhaps this is the most biologically reasonable definition of race ... while of course acknowledging that it creates a crapload more checkboxes than any census form could reasonably accommodate and looks next to nothing like the traditional races of racists, but that's what happens when you use reality and not racist ideology as your basis?

Also regarding the other comments here ... there might not be an inconsistency between the two data sets/models. There is, if you look at the above tree-graph, a "Europe" cluster, i.e. a node branching to European populations, also a "Middle East" and "East Asia" cluster, and a huge "West Africa" cluster. Keep also in mind most "Black Americans" are from West African origin. So there are actually four clusters that decently approximate the four "United States Racial Hierarchy Races", and thus having "Self-Identified Race/Ethnicity" match clusters is not wrong.

The trouble is that they are at different nodal depths, and there are larger groups that also include some of, but not all of, groups corresponding to what may have been lumped under a different heading in trying to fit everyone to the US Racial Hierarchy Model. Such as all Africans as Blacks, which actually by this nodal classification would necessitate taking almost everyone as Black since Europeans are filed under East Africans as a sub-group! (The only ones that would not be would be those two green lines on the bottom ... and I can't read the labels.)

In other words, this picture both supports and rejects the "traditional racial model" used in the United States. As with sooooo many things, the truth behind these matters is not entirely what either set of duelling, polarized, and ideological partisans want to make it out to be.


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Help me identify this Beetle sp?
I observed many beetles like this in Pune/India in the beginning of rainy season. It was dark green in color with white spots and not too much shiny like many other beetles. Size is about 2cm to 3cm.

It is certainly a scarab, in subfamily Cetoniinae. It looks very much like a White Spotted Fruit Chafer, Mausoleopsis amabilis http://www.projectnoah.org/spottings/11819281

Thanks for above link from which I found this species (Protaetia alboguttata). It seems correct identification.


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Do all cells have the same DNA?
According to genome.gov, All the cells in a person's body have the same DNA.
I understand that the main reason parents and children have different genomes is because of random mixing of 2 genomes, but that there are also very small differences caused by random mutations.
If all of a person's cells have identical genomes, then does that mean that random mutations only occur in gametes?
I also understand that if sunlight hits my arm, it can cause random mutations.
So do all cells in a person's body really have the same DNA?

Also see : https://biology.stackexchange.com/questions/77181/how-much-variation-is-there-between-dna-molecules-from-the-same-organism

All cells in a person’s body have roughly the same DNA. As you point out correctly, mutations can happen in any cell at any time. They are frequently caused by

UV radiation
Chemicals (think of the correlation between the development of lung cancer and smoking)
Replication of DNA during cell division
Integration of foreign (e. g. viral) genomic material
On purpose by the body’s own enzymes

That last point brings us to cells of the immune system, some of which (classically T- and B- Lymphocytes, but there is emerging evidence for others) generate variance within their genomic DNA on purpose.
Red blood cells lack a nucleus altogether.
Gametes only have half the body’s genome, as you already pointed out.
Finally, although having the same base sequence, epigenetic modification of DNA molecules by, for example, Methylation makes DNA chemically different even between cells of the same type.

Mutations do also happen during mitosis, hence leading to cell lineages in your body to differ genetically by some mutations. While the vast majority of these mutations have no significant effec ton the individual health, some of these mutations may lead to serious health issues such as cancer. Also, you might want to consider that some cells are anucleated (red blood cells typically) and hence do not contain any nuclear DNA.
So, in short, the statement

All the cells in a person's body have the same DNA

is a "good approximation" but is not "exactly correct"!


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Want to know which insect it is? I often found it in washroom. Is it dangerous and how to control it
This insect found in the wash room.  Its so fast and disappears once someone enters the washroom.  Is it dangerous?  Whats name of this insect.  How to control this insect

Could you please edit your question and add your geographical location and the size range of this animal? Can you estimate the number of legs?

That is a house centipede, Scutigera coleoptrata https://en.wikipedia.org/wiki/Scutigera_coleoptrata
They are harmless, unless you are a cockroach or termite. People find them unpleasant and creepy, because they run fast, but they are predators that prey on pests in your home.
https://www.familyhandyman.com/pest-control/heres-why-you-should-never-kill-a-house-centipede/

They do seem to have a rather nasty bite. Maybe it is nice to add that to your answer?

No they don't. It may be possible that 1 encounter in a million ends up in a bite, when people are handling them, but I have never heard of it. People have an irrational fear of these completely harmless creatures, and the last thing you would need to say it that there is a minuscule chance that a huge one could bite if you put it in your hands and squeeze it.


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Sequencing inaccurate at the primer site
The times I have sent a sample to sequence, both the forward and the reverse primer sites, show high inaccuracy while the rest of the gene is correctly sequenced. Because of this, the sequences of my in silico construct and the sequenced sample do not align in this section; but they do align at the rest of the gene almost 100%.
Is there a reason for this? Is this simply a sequencing artifact or is should I trust the sequenced sample and assume that the primer sites have mutated?

The beginning is always garbage, you can safely disregard. Though, the fact that you have a sequencing result at all means the 3' end of your primer matches the template.

The very extremities of sequencing reads obtained by most if not all sequencing technologies are usually of lower quality, though more often so in the 5' region. You should disregard this data, or better yet design additional primers further away to encapsulate that region too if you desperately need it.
Below is a fairly typical output from FASTQC analysis of Illumina sequencing data. You can see how the quality is at its peak in the middle of the read (base index on the x axis. You'd likely see a similar thing for Sanger sequencing which is presumably what you're using.

What would a good score mean? and what would a good score be? I imagine from the colors that anything on green is good, but just to know a bit more about sequencing.

It can vary by sequencing technology, but most techs these days use something called “Phred-33” scoring. It’s a logarithmic relationship that roughly speaking means a Phred score of 30 (on the Y axis in the pic above) means there’s only a 1 in 1000 chance that base was called incorrectly. Most people accept 30 as a reasonable quality for sequencing, also helped by the fact that you have many millions of overlapping reads (in NGS), so even if a base is miscalled in 1 read, chances are there are many other reads you can refer to that would have the correct call.


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Why analyse transcriptome instead of proteome?
Analysing the transcriptome (RNA-Seq, microarrays, qPCR etc) is probably the most widely used technology to assess gene expression and dynamic cellular processes. The results are then extrapolated (functional analyses, GO etc) to infer biological cellular consequences. RNAs are really only the middle-man. Presence of an mRNA doesn't necessarily mean that it will become a protein. It could be degraded by microRNAs etc. before translation. It is eventually the protein that are actually causal to a biological change.
So, my question is why not just go directly to the proteins. Why not just extract the proteins and sequence them, quantify them, analyse and draw conclusions? What are the compelling arguments to study the transcriptome to understand biological processes?

Another thing that is not directly related to your cellular process premise, but is nonetheless a positive of RNA-Seq: it also gives you coding and protein sequences at a cost far less than proteomics or genome sequencing, so it's useful for phylogenetics/phylogenomics

@NatWH, A good point. We also need sequence databases to search mass spectrometry-based proteomics data. In the absence of genomic data many groups use RNA-seq data to build this sequence database so they can then use MS.

Q: Why not just extract the proteins…

A: It’s not just a question of extracting the proteins, you would need to separate them and then isolate each of them. There is currently no practical way to do this for say, 10,000 proteins, which in any case may have multiple forms. The beauty of the RNAseq method is that it does not require physical separation or isolation of transcripts.
An approach more likely to be useful is to identify and quantify the proteins in situ, but this is still some way off having the comprehensiveness and sensitivity required.

Q: …sequence them…

A: Protein sequencing is slow and difficult. It cannot be applied on a mass scale, unlike sequencing of DNA copies of RNA transcripts. Other methods of identification based on physical behaviour (migration or elution position) are more promising, and the direction that is likely to be followed.

Q: …quantify them…

A: Even that is difficult, when you are eluting proteins from gels, for example. In contast, RNAseq methodology just counts transcripts. (But the likely direction this will go is quantitation by peak height, without separation or isolation, as with metabolomics, or by the intensity of some signal from the protein immobilized in the gel, staining of something more sophisticated.)
So, in general, you do protein analysis on particular individual proteins of interest to you, whereas you can do RNAseq analysis on all the transcripts in a biological sample, and then go fishing (among the results, and afterwards on the lake if that’s your thing).

There are no methods that will separate, say, 10,000 proteins  gel electrophoresis can easily separate this number of proteins. Liquid chromatography can too. Detecting intact proteins is currently low-throughput but LC-MS on peptides can provide quantitative data for 1000's of proteins, the ability to detect PTMs is a feature not a bug.

@Michael_A — technically you may be right (or partly so), but in the context of this question from a naive list member I think your comment is more likely to confuse than enlighten. I'll rewrite my answer in a way that deals with your point without diluting the explanation. But it will have to wait another day.

@Michael_A  — I have modified my answer to address the points you made. At some time I may modify it further with a consideration of how technological breakthroughs influence science, and the references to the current state of proteomics.

Why not just extract the proteins and sequence them, quantify them,
  analyse and draw conclusions?

Because proteomics is really hard. To provide one example, there is no protein equivalent of PCR. That means there is no simple way to select and amplify a particular protein from a complex mixture. The invention of PCR was central to the rapid advances in genomics over the last 40 years.
Mass spectrometry is the primary tool for high throughput proteomics and mass spec analyses are still very difficult to run, and even more difficult to interpret.

While you are correct that 'the end output' is always protein and that functional analysis on the mRNA level can ignore things translational control, there good reasons to analyse the transcriptome:
1) Like you said a lot can happen with mRNA: it can be degraded, translated or also be repressed for a time until it's activated again. Most of these control processes have pretty strong effect on the 'final protein output' but are much easier to study on the mRNA/transcriptome level (since that is where they happen).
2) Analysing the transcriptome on a genome wide level is technically relatively easy: Sequencing technology is pretty advanced by now and there are many different protocols established to look not only at expression levels of individual mRNAs but also other things like stability, processing (i.e. splicing or polyadenylation) and also translation of mRNA. All of this can also be done with relatively low material input.
Protein analysis on the other requires the use of mass-spectrometry which is not necessarily as powerful or sensitive as sequencing.

I think it's useful to bear in mind that the transcriptome does consist of non-protein coding transcripts such as miRNA, and that while protein is largely regulated, the end product is not always protein. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177046/

What are the compelling arguments to study the transcriptome to understand biological processes?
There are compelling arguments to study the transcriptome but they depend on the research question. Research that focuses on the activation of transcription factors should use transcriptome data as should research into RNA processing events (splicing, pre-mRNA processing, stability). You also want transcript data when studying RNA transcripts that don't encode proteins.
I don't think there are compelling biological arguments for studying the transcriptome when you want to know about the expression of protein-coding genes in tissues or cells. You should focus on proteins as they are the final step in the expression of protein-coding genes. The correspondence between the levels of protein-coding transcripts and their protein can be excellent but may also be very poor. Transcript data can't segregate these groups. In global estimates, transcript levels only explain around half of the variation in protein levels. I think that level of inaccuracy unacceptable when there's a viable alternative.
Why not just extract the proteins and quantify them?
There are physical and historic limitations to global quantification of proteins. I've compiled a couple limitations that I consider to be most important. Mass spectrometry (MS) is the current method of choice for high-throughput protein quantification. Methods such as Edman sequencing or immunological detection have much lower through-put.
There are physical limitations that currently stop MS from performing quantitative global measurements using intact proteins. That's very unfortunate. Global measurements are currently performed by quantifying peptides from digested proteins using a liquid chromatograpy system to feed the MS with peptides (LC-MS). The peptides are identified and then assigned to a protein or group of proteins. The end results are reliable and most will resolve to individual protein identifications. Some peptides will only resolve to identify a group of proteins. This is a minor limitation in most instances.
Making global measurements of protein quantities has only become possible in the last decade while global measurements have only become routine with the advent of ultra-high performance LC paired to the newest mass spectrometers. Many academic researchers will have access to this technology via their local mass spectrometry facility but most won't realise it. This newness is a big part of the reason it's less common.
Summary
I think LC-MS quantification of proteins will be used in place of transcript data more often over the next couple of years. This is due to the ability of  as current LC-MS instruments provide better answers in biological systems that require protein-level information. Reviewers will start to demand it. I think within the next decade high-performance LC-MS could become cheap enough to even replace lower throughput immunological techniques such as immunoblotting and immunofluorescence.

There is one aspect that has not been detailed: a transcriptome is way cheaper than a proteome. Analyse one single protein in LC-MS/MS can cost as much as a transcriptome. And if you belong to those small underfunded groups that work on non-model organisms which are really interesting but not really useful for curing cancer, then you have no choice.


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Is egg white lysozyme different from bacterial lysozyme?
Someone told me that microbial lysozyme has effect on gram negative bacteria but egg white lysozyme only affect gram positive bacteria. Is it true?

Whoever knows the answer to this question knows it by (a) having done the necessary experiments, or (b) having read the reports of those who had done the necessary experiments. Start with 'b' and if you don't find any such reports, continue with 'a.'

I searched about documents to prove that but i can’t find any one

Search the PubMed literature database . . .

PubMed query: "lysozyme"[Title] returns 8673 papers (many of which contain useful data about the activities of bacterial- and chicken-type lysozyme/muramidase against Gram-positive and Gram-negative bacteria).
For example, Gajda & Bugla-Płoskońska (2014, Postepy Hig Med Dosw 21, 1501-1515) write:

Lysozyme (LZ, muramidase, N-acetylmuramylhydrolase) is a protein occuring in animals, plants, bacteria and viruses.
Lysozyme hydrolyzes the β-1,4 glycosidic bonds between N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) of cell
  wall peptidoglycan (PG) in Gram-positive and Gram-negative
  bacteria.
In the animal kingdom, three muramidase types have been
  identified: the c-type (chicken type), the g-type (goose-type) and the
  i-type (invertebrates).
Muramidase shows bactericidal activity mainly against Gram-positive bacteria. Cytolytic activity against cells of Gram-negative bacteria
  has not been proved.

Lysozyme hydrolyzes bacterial cell walls, which is why its muramidase activity is more effective against Gram-positive than Gram-negative bacteria, for the former have thicker cell walls. Whether or not there is any difference in the effectiveness between the bacterial- and chicken-type lysozyme can be found in the papers; i have not read them.
But one of the 8673 papers is titled Hen egg white lysozyme permeabilizes Escherichia coli outer and inner membranes (Derde et al., 2013, J Agric Food Chem. 16: 9922-9929).
The quick-and-dirty answer to the question, is it true that bacterial lysozyme affects Gram-negative bacteria but hen-egg (chicken-type) lysozyme only affects Gram-positive bacteria? is: No.
The 'slow-and-clean' answer can be found in those 8673 papers.

Thank you for your help, I already found this answer but i need to know the difference of the two type of lysozyme: a. Microbial lysozyme b. Egg white lysozyme on their effect on bacteria (is microbial lysozyme affect gram negative bacteria and egg lysozyme doesn’t ?

@MahmoudOraby i edited my answer; you have everything you need to find the answer for yourself; or you can wait until someone else gives you a more detailed and comprehensive answer.

@MahmoudOraby if you read 100 abstracts of "lysozyme" papers a day---which is doable---you will become lysozyme expert in 3 months (if that's what you would like to be). Of course, you can narrow your PubMed "lysozyme" search using logical operators (and, or) and additional keywords, and filter the results by publication type (e.g., Review)---this way you can get to the bottom of the pit faster . . .

already I began to do that


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Can low melatonin levels and/or LED lights cause or exacerbate macular degeneration?
I have two questions that may or may not be interconnected. My first question is:
Does melatonin prevent macular degeneration? Could low melatonin levels (caused by blue-rich light exposure in the evening and night and/or by insuffient sleep) heighten the risk for macular degeneration due to shorter amount of time that melatonin scavenges free radicals in the retina?

Evidence is conflicting as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study on 446 subjects found it does not [1]. Other research, however, has shown high-energy visible light ("blue wavelengths") may contribute to age-related macular degeneration [2 and 3].
Data indicates that melatonin, being an efficient antioxidant with antinitridergic properties, has a promising role in the treatment and management of glaucoma. Melatonin could protect the ocular tissues against disorders like glaucoma, age-related macular degeneration, retinopathy of prematurity, photo-keratitis and cataracts [4].
However, melatonin secretion is inhibited by short or low quality sleep and by the ubiquitous blue-rich light exposure in the evening and night, hence for many people melatonin secretion starts as late as 90 minutes after falling asleep (i.e. 90 minutes after the last exposure to shorter visible spectrum wavelengths). As a consequence, melatonin has less time to function as an antioxidant in the body in general (which has been proved to result in higher cancer incidence) and also in the eye. When people are not exposed to blue wavelengths in the evening (e.g. by using firelight or dimmed incandescent bulbs or wearing red glasses) melatonin secretion starts roughly 90 minutes before sleep so melatonin has more time to do its antioxidant work.

My second question is about the relationship between macular degeneration and LED lights.
Could LED lights also increase the risk for macular degeneration?

Typically, LED lights (CCT = 4000 K) have a maximum peak at around 451 nm and a minimum in the 460-500 nm range (as is shown in their spectral power distribution of such LED lights below).

Melanopsin that controls pupilary reflex (pupil constriction), however, has maximum sensitivity around 479 nm - right in the LED spectral power distribution's (SPD) minimum. Could it be that due to this gap in SPD the pupil does not constrict enough and hence allows more of this blue rich light into the eye that as a result generates more free radicals and contributes to macular degeneration? Could this in combination with low sleep quality contribute to the onset of macular degeneration as LED (and lack of sleep) are widespread?
PS: I vaguely understood that at the moment it might be hard to answer some questions regarding melanopsin, but I am not sure how much it is related to my question. "It would be desirable to be able to quantify light as experienced by non-visual systems (melanopsin) using a single, one-dimensional unit (the equivalent of photopic lux). Achieving this for lights of divergent spectral content, however, awaits elucidation of a suitable spectral weighting function" [5]

Thanks for all of the prior research you have done. Can you maybe clarify what the actual question you are asking is, edit that question into your title, and make your question more prominent in the body? As-is, I think your background information, while appreciated, is masking what you are getting at, and many people won't take the time to read your whole question.

Thank you, I agree with you, will clarify it immediately!

@BryanKrause is it better now? I am sorry it was unclear.


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Thousands of Reporters Integrated in Parallel (TRIP) barcodes
Has anyone worked with constructing barcodes for TRIP? How does constructing of barcodes work in general? I don't seem to be able to grasp the basics of constructing these barcodes.

From the paper and user manual it seems that barcodes are random sequences of pre-defined length of 16-20bp ± 1bp. On data analysis step they are combined and all barcodes 2 Hamming distance apart (it means that two words have difference in one letter from each other) will be discarded from the list of genuine barcodes.


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DNA preservation at room temperature
I am considering preserving the DNA of a family member who passed away. The funeral home offers a service called DNA Memories from a Canadian company (CG Labs). They have two options: Store the DNA in their secure temperature-controlled facility, or "home DNA banking", where they somehow preserve the DNA such that it can be stored without damage "indefinitely", at room temperature. This is how they describe the technology:
"The  DNA is bound to a substrate and sealed under nitrogen gas with out patent pending process. This process allows the DNA to remain in a state of suspended animation and if the vial remains sealed the DNA has an indefinite shelf life. The DNA Memorial Home Banking may be banked in non extreme conditions and room temperature for future testing at home."
My question is basically this: Is there any scientific merit to their claims (i.e. is there anything peer-reviewed on the subject of room-temperature DNA preservation for many years, using technology such as the one they describe)? Can DNA preserved in such a way really be tested later in regular DNA testing labs (or will I need a specialized lab that knows how to deal with this unique process)? Is there any possibility of a full sequencing later of DNA stored in such a fashion?

If you would like to sequence this family member's DNA, why not sequence a sample now? Without a link, I'm not sure how to evaluate their process, but I would be skeptical. When I'm banking a DNA sample for future, unknown testing, I store it at -80 C.

I worked with museum specimens that were 40 years old, and dried, they were fine. They sequenced the Neanderthal genome. In my experience, DNA can be safely stored at room temperature.

DNA is already a pretty stable molecule. Storing it under N2 sounds like they have it precipitated form (i.e. lyophilised) - I would expect lyophilised DNA in a N2-only enviroment to last for a very long time. The biggest issue for using it later would probably be UV light exposure and physical fragmentation (which isn't a big problem for sequencing though).


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What's a good reference for learning about recombinant proteins?
I'm looking for books and articles that can bring me up to speed on the design, expression, and purification of mammalian proteins in recombinant systems, both in E. coli and in more complex systems like CHO or Sf9 cells. I have a weak but functional background in general molecular biology.

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!

i would start by searching PubMed literature database for relevant articles using this query:
"protein"[Title/Abstract] and "expression"[Title/Abstract] and "purification"[Title/Abstract] and "recombinant"[Title/Abstract] and "mammalian"[Title/Abstract] and ("E. coli"[Title/Abstract] or "CHO"[Title/Abstract] or "Sf9"[Title/Abstract])

which returns 116 articles (including 7 reviews).

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

@LinuxBlanket Except that it is not an answer but a suggestion as to how to find an answer.

@David "why not upvote it" - "it" was referred to the question, not the answer. I wanted to incite the answerer to upvote the question. I didn't express myself clearly, my bad!


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The size of the Triceratops specimen Lane in the Houston Museum of Natural Science
In 2012 the Houston Museum of Natural Science published they discovered an almost complete fossil of Triceratops including fossilized skin, see HMNS post, and nicknamed it "Lane".
I am interested to know the size of the Triceratops specimen Lane and in particular: total body length (TBL), total head length including the frill (THL) and brow (superorbital) horns cores length. Estimation of weight would also be great but I doubt if there are any.


text:
Searching a fructose degrading bacteria
my question is do you know a fructose degrading bacteria?

Wich is straitforward to use and cultivate?

Wich shouldn't create excrements, that can't be removed simple.

Welcome to SE Biology. As a new contributor we do not wish to discourage you, but your question falls somewhat short of what is expected here. You would benefit from reading the help on how to ask questions where you will see that good questions are of general interest, provide detail and context, and show evidence that that poster has done research of his own before asking. Do some internet searching and then modify your question to tell us what you have found about fructose degrading bacteria and what you still need to know.

Many bacteria use fructose as the growth substrate but there is a small group of bacteria called fructophilic lactic acid bacteria (FLAB), for which fructose is the optimal growth substrate.
FLAB includes several species of the genus Fructobacillus (F. tropaeoli, F. pseudoficulneus, F. ficulneus, F. fructosus, Frucobacillus durionis) and Lactobacillus (Lactobacillus apinorum, Lactobacillus kunkeei, Lactobacillus florum), isolated from fructose-rich environments, including flowers, fruits, fermented fruits, and the guts of insects that feed on plants rich in fructose.
FLAB can be further differentiated into obligately and facultatively fructophilic, based on their preference for fructose over glucose as the growth substrate.

Endo et al. (2018) Fructophilic lactic acid bacteria, a unique group of fructose-fermenting microbes. Appl Environ Microbiol. 84: e01290-18.

that sounds great, I will research soon. Thanks for the answer.


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In endochondral bone formation, why does only hyaline cartilage get ossified to form bone?
There are three types of cartilage: hyaline, fibrous and elastic cartilage.
Fibrous cartilage does not have perichondrium...so it does not take part in ossification because perichondrium needs to develop into periosteum.
Hyaline cartilage has more matrix in comparison to elastic cartilage. Hence, during ossification the quicker spreading of calcification of the matrix will lead to the death of the chondrocytes which will develop into osteoprogenitor cells. Is my theory correct?

'... calcification of the matrix will lead to the death of the chondrocytes which will develop into osteoprogenitor cells.' How can dead cells develop into living ones?

yes this is correct, i think hyline cartilage gets transformed to bone more quickly due to the fact that is has the matrix which is closest to bone in terms of density, also the cells are located more closely, therefore it is easier to convert this tissue to bone.

Welcome to Biology.SE! This sounds reasonable, but without supporting references only an expert in this area can evaluate your answer. Consequently, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!