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Sleep deprivation relation to growth rate and mental health in adolescence
Do sleep deprivation and its timing affect growth rate and mental health in adolescents? If so how much sleep is enough for teenagers?

Welcome to SE Biology. I am afraid that personal medical questions and health advice are off-topic here, and your question would seem to be asking for health advice. Please see the Help Centre.

@David i still think if Daulet reformulate this question as question with general meaning, I ll be able to answer this question.

@L.Diago — Then you need to explain to him how you think his question needs reformulating. My own opinion stands. If there is any SE site this is relevant to it would be Medical Sciences, but, like this site, that is supposed to be for professionals and serious students.

@L.Diago — I noticed that the poster used the "health" tag. The summary of that is worth reading: "Health and medicine questions are off-topic unless dealing with the biology underlying health and medicine. Please carefully explore the tour, help centre, and meta before posting health and medicine questions. Health is a physiological state of well-being referring to the (ab)normality of the cellular or organismal physiology."

@David but it can be take from circadian physiology point of view. Sleep deprivation And mental health Is pretty common topic in chronobiology.

@L.Diago — Well make and state your assumption of what a good question would be and give a good technical answer. My vote is only one of five needed to close a question.

@L.Diago Thank you very much for editing my question! : -)

@Daulet Aybaz i ll try produce relevant answer as soon as possible.

@L.Diago I would appreciate it!

@DauletAybaz i am sorry that it is taking so long, but i was really surprice about lack of articles on growth hormone regulation associated with sleep. Just saying that i wont ditch you.

@L.Diago Thank you for your work! I really appreciate it and waiting for your answer and info)

A couple of papers (from the same group, it seems) defines sleep deprivation in adolescents as less than 6hr of sleep within a month. They found that sleep deprivation increases health risks, importantly depression (which in turns increases sleep deprivation).

I think it needs to be pointed out, that defining sleep deprivation as less than 6hr and finding some detrimental effects says absolutely nothing about whether more than 6hr is enough.


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Nature versus nurture regarding aggression in specific dog breeds
A week ago I was bitten in my face by a dog that originally came from an asylum. That dog is half Rottweiler. Some people claim that the history of the dog is probably different from what the asylum thinks or says, whereas other people claim that Rottweilers or male Rottweilers are unreliable. But let's not focus on this single occurrence and ask the wider question:
Is there scientific evidence to indicate that there are certain breeds that produce significant numbers of dogs that are inherently and unreliably aggressive, or is such aggression usually the consequence of how their owners raised them?

How are dogs political? Anyway, we don't do political discussions here — they get vacuumed up very quickly.

@David An answer to the question would be an argument in the political debate whether certain dog breeds should be banned, as was once the case in Belgium.

I see. But, as I said, this SE is only for objective biology questions and objective answers. In general I would advise not anticipating trouble with your post — it is more likely to provoke it than otherwise. Trust in the good sense of members until they prove otherwise, and then flag any inappropriate responses to the moderators.

It seems that there are some important differences in dog aggression depending on the dog breed (towards strangers, owners, and other dogs):

That being said, it seems that a significant proportion of a dog's behavior can be due to its environment (training, etc), according to a study, this 'nurture' component might explain up to 80% in the variation in aggression (which should be considered when interpreting the other study I cite).

For discriminating viewers: the error bars indicate a 95% confidence interval, i.e. the range of values for which we can be 95% certain to contain the true mean of the population. Notice the error bars are quite wide. Notice also the scale bars; we are always talking about < 1% of dogs (1-3 out of 138 dogs on average) so I would be wary of these pretty tiny differences. We're talking about being hit by lightning vs. winning the lottery statistics here. Interpret them with a grain of salt!

For even more discriminating viewers: Notice the Y-scale represents a value that can vary in the [0,4] interval, which is the interval used in this particular technique (0-no aggression, 4-most aggression). So, these are not 'pretty tiny differences'. Basic statistics are easy to be misinterpreted. More info: https://sci-hub.tw/10.2460/javma.2003.223.1293

There are also very few other studies that replicate any dog breed findings. I would be as cautious as the authors themselves, who in their own words state that "the substantial within-breed variation in C-BARQ scores observed in this study suggests that it is inappropriate to make predictions about a given dog’s propensity for aggressive behavior based solely on its breed." And remember that the data is based on subjective questionnaire reporting online, which is difficult to gauge as trustworthy or true to reality, especially since we are talking about pets!

You're on your right to be cautious, but 259 other papers citing this study are not "very few": https://bit.ly/31WZtDH - in any scientific field (biology specially) that is quite a significant number of citations. I quote another study citing the paper: "questionnaire surveys provide more detailed information about the dog's behaviour than behavioural tests, especially about low-frequency behaviours (Duffy et al., 2008)". (https://bit.ly/2MmDqzO). I'm sure the study is not perfect, but criticizing its statistics/design without knowledge of the matter is not very scientific either.

There is another study, in addition to that cited by @TumbiSapichu, that establishes a genetic component in canine aggression. This is: Zapata et al. (2016) BMC Genomics 17:572 and is entitled Genetic mapping of canine fear and aggression.
The study did not set out to establish which breeds, if any, are most aggressive, but started from the proposition that there might be a genetic component in canine aggression, and tested this by a genome-wide association (GWA) study on one cohort of different breeds. This established certain candidate genes, which were tested — and confirmed — on a second cohort. The authors of the paper conclude:

“We have mapped many canine fear and aggression traits to single haplotypes at the GNAT3-CD36 and IGSF1 loci. CD36 is widely expressed, but areas of the amygdala and hypothalamus are among the brain regions with highest enrichment; and CD36-knockout mice are known to have significantly increased anxiety and aggression. Both of the other genes have very high tissue-specificity and are very abundantly expressed in brain regions that comprise the core anatomy of fear and aggression – the amygdala to hypothalamic-pituitary-adrenal (HPA) axis. We propose that reduced-fear variants at these loci may have been involved in the domestication process.”

I appreciate that the reader may wish to see a graphic showing that Rottweilers are more aggressive than Yorkies, for example. However the paper clearly answers in the positive the question of whether there is a genetic component in canine aggression, and the paper has 20 pages and eight figures for anyone who wishes to tease out information regarding specific breeds. (I do not own a dog, so lack the incentive to do so myself.)

source: Stack Exchange

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

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same osmotic pressure of different solution
For example, There is a sugar solution with concentration $A_{1}$, how to determine the concentration of a NaCl solution which produce same osmotic pressure as the previous sugar solution toward animal's cell?
Is this ratio various between different kind of cells?
NOTE: the unit of concentration is not important between mass/vol or mol/vol. Because when one is known, the other is easy to compute.

Is A1 known? If yes, have you taken a look at this video?

@SPr, Yes, it is known.

This is a simple chemistry question. The answer is 0.5A₁ but I won't explain why. Read about colligative properties. I am VTCing this as a homework/General Chemistry question.

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


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Why is there no solid evidence (histological, fMRI) that the vestibular hair cells of the inner ear contribute to 53% of the respiratory drive?
There are these papers which strongly imply that the inner ear hair cells, and not the medulla, is primarily the driving factor in the CO2 drive reflex
https://www.ncbi.nlm.nih.gov/pubmed/21130842
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988803/
But every fMRI study done on chemoreceptors has shown only areas of the brain and carotid bodies light up in response to CO2. I could not find any fMRI study papers showing that the inner ears light up in response to CO2 or any histological evidence that the hair cells of the inner ear are chemosensitive and play a larger role in chemosensation than the brain like these studies are trying to imply. It is said the central chemoreceptors in the brain contribute to 85% of the CO2 drive reflex and the peripheral chemoreceptors contribute 15%, which seems to leave little room for the inner ear hair cells to play such a vital and significant part.

I note the two papers from 2011 & 2013 are from an overlapping set of authors, and have hardly any citations outside of later papers involving one or more of these authors.  It looks like very little further research in this area has been reported.


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Why do we need to amplify DNA sequences?
I am learning about biotechnology. I have no education in biology or chemistry and am simply interested in the subject of biotechnology.
I am wondering why we need to have multiple copies of a piece of DNA in order to do something with it (ie. PCR)? Why is one piece of DNA not enough? Is machinery not precise enough to work with one piece of a DNA sequence in order to do something with it?
I can understand that an experiment may fail. In that case, make 8-16 copies for assurance. But why an extraordinary (billions) amount of copies? What practical use does it have? What applications require there to be an extraordinary amount of DNA to be succesful? Do the billions of copies just increase the speed of the experiment by being able to quickly "fish out" a piece of DNA? I just can't quite grasp the idea.

Although your question about DNA has been answered, you need to be aware of the general limits of detection of molecules in the lab. If you thought you could detect one molecule of DNA, think about detecting one molecule of glucose. How much would that weigh? You can find the answer by reflecting on Avagadro's number — the number of atoms in a mole of a compound. This has a value of about 6 x 10^23, so there would be that many molecules in 180 g glucose! Catch one!

This is a question I also remember wondering about when I was younger in school. Now as a professional it's way too obvious to even explain. But i think it's an important and common question, which warrants an example or two from common daily lab practice.
Preface
You have to understand that DNA is a molecule. It's really tiny. It's not trivial to work precisely with it, nor detect it or discriminate two different pieces of DNA from each other, let along sequencing them. We make a lot of DNA through amplification so that we can prepare a sufficient amount to make reactions with.
Visualization
We usually make DNA visible by using chemical dyes that emit light (fluorophores) or incorporated radioactive pieces to make the DNA visible.
Here's a common case in the lab: we need to get enough DNA to use in subsequent reactions. When we work with DNA it is very rare that we obtain exactly what we want 100% of the time, or perfect yield. For example, we want to cut a piece of DNA once. But we have scissors (i.e. restriction enzymes) that will chop up the DNA multiple times, especially when we leave the reaction going too long. What we do is take 100 units of DNA, subject them to the reaction, and then view the results using electrophoresis using an agarose gel, for instance. We can then see 40 units of uncut DNA, 30 units of single cut DNA, and some 30 units of DNA cut multiple times (2+ times, so they are small fragments). We need enough single cut DNA to proceed with the next reaction, with full knowledge that there are no contaminating chunks of DNA. Typically there are many reactions in a row that we do to achieve anything in the lab. Cloning, in vitro amplification, sequencing, gene editing, preparing genes for transgenesis, creating RNAi probes, what have you.
More is better
Another case: if you want to know the sequence of DNA, you must sequence it. However, sequencing is imperfect and errors occur. To be sure, we re-sequence the same DNA many times to get a confident picture of what the sequence is like, beyond reasonable doubt. Sequencing DNA ten times is really more reliable than sequencing it once. This could be because of how the molecules behave in solution, or because of degradation, or tens of other things. You must understand this is also not specific to sequencing; a lot of reactions follow the same logic.
Amplification as a specification tool
By using primers in PCR, we can make sure we are obtaining what we want. In principle, this means that we can make a gajillion copies of something we are interested in (e.g. a gene), even from a single strand of DNA which may contain things we are uninterested in (e.g. the rest of the genome).
Some thoughts
This answer is certainly not extensive, but I hope it's a primer for you to understand that DNA work is just really smart nanotechnology, and we are not yet at the level of performing nanotechnology on single molecules, with full confidence, precision or efficacy. On the daily, we need enough to see it with our eyes so we amplify and react it with intercalating dyes to make them visible to the naked eye!

Thank you for the succinct answer. I was failing to understand the precision of current nanotechnology, and your practical examples (which sound really fun) really brought the point home.


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Are all of my ancestors from 400 million years ago fish?
Say you have your family tree for the last 400 million years or so, back to the Devonian, the age of fishes. You take the set of ancestors that are about 400 million years old (which will be across multiple generations). The question is are they all fish?
Or, is it more complex than that? Can there somehow be non-fish in that set?
Note added later: this question is not a duplicate of another question.
In the context of that other question, howewever, my question can be stated as "Is Dawkins correct in stating that my 185th million ancestor was definitely a fish, with no exceptions?"

Possible duplicate of Same 185th million grandfather?

I would say no, it's not the same question.

Yes they all were because there weren't any land vertebrates, vertebrates were all fish at 400 million years ago.
It is a close call based on fossil evidence from 395 million years ago, there are footprints of 3 meter tetrapods from littoral/seaside fossils. https://www.sciencedaily.com/releases/2010/01/100107114420.htm
The earliest land vertebrate skeleton is from 375 million years ago. https://en.wikipedia.org/wiki/Tiktaalik

It is technically still a fish, so probably yes, the ancestral species of all land vertebrates were still fish. There are various experimental early quadrupeds, some with 6 fingers, which are cool reading.
They still exist in the form of lungfish.
Here are images of the earliest land vertebrates

It is worth noting the problems with the term "fish" . Depending on how you use the term humans can also be fish.


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How far can a human see at night?
I am not talking about seeing in total darkness, which I understand is not possible. I am looking more about a question how far can a human see during starry night or with half moon/full moon. I tried googling for this, but found no useful results.
EDIT I think I need to clarify: I am thinking more in terms of immediate surroundings. I understand we can a source of light from afar, but what about a tree on a flat land - from how far would we see it in star light?

A better, more scientific way to ask this question would be to ask about visual acuity as a function of luminance... there is no meaningful way to answer your title question without specifying other key parameters.

You would need to further specify it, for example, at a certain lumination (half-moon), from how far you could recognize a tree as an oak (from the shape of its leaves). Anyway, half-moon can be quite bright...

Hmm.. I would like to build some kind of intuition about this, not exactly have a formula. Would I be able to discern a tree shape from star light only in an empty field? From what distance? How about full moon? Are there any resources I could take a look at or examples? Examples would likely work best for me.

At night you can actually see further than during the day. At night you can see stars that are many light years away, but during the day the furthest thing you can see is probably the sun, which is 8 light minutes away. There's probably no definite answer because the brighter and bigger the object (and the darker the surrounding and the clearer the air), the greater the distance from which you can see it.
According to Sky and Telescope, the most remote stars (as part of Andromeda Galaxy) you can see with a naked eye are 2.5 millions light years away.
Talking about the objects on earth, at half-moon, you could see to "the end," that is to the horizon.

Thanks a lot for the answer, I clarified my question.

With clear, dark skies (no urban light pollution), about 2.5 million light years.  That's the distance to the Andromeda galaxy, which is visible (in the northern hemisphere) with ordinary visual acuity: https://en.wikipedia.org/wiki/Andromeda_Galaxy#Amateur_observing
Vision does not depend on distance, but on the brightness of the things being viewed, and their size.  That is, we see stars as points because their diameter is too small to resolve (angular resolution) but they still put out a lot of photons.  We see Andromeda as a fuzzy patch of light, because it is composed of lots of stars spread over a large distance.
For more ordinary things, it depends on the amount of light, and the size. Flying in a small plane on a clear winter night with half moon or more, it's possible to see snowcapped mountains 50 miles (80 km) or more distant.

Thanks a lot for the answer, I clarified my question.

The clarification doesn't really help.  What do you mean by seeing the tree?  Do you need to see the light reflected from it, or is it sufficient to see the shape of the tree blocking starlight?  You could probably calculate an approximate answer to the first case from intensity of starlight * reflective index of the tree * the inverse square of the distance, and comparing it to visual acuity.

OK, to clarify further: In an empty field, with star light, from what distance could I discern a shape of a tree? How about a person? And how about with a half moon or full moon?


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How much DNA (or genes) do homo-sapiens and ursus arctos (brown bear) share?
How much DNA (or genes) do homo-sapiens and ursus arctos (brown bear) share? There are articles online that indicate that humans share xxx% of DNA with Chimpanzees, bananas, and other assorted organisms, but I can not find how much humans share with brown bears.

These percentage measures do not make a lot of sense. Humans also share a significant number of genes with bacteria. If you want to make comparisons, you should do an extensive analysis of the whole genome. A seemingly minor change in the genome can cause a drastic change in the traits.

timetree.org is a good place to start exploring questions like this. You can put in 'human' and 'brown bear' and it will find a whole bunch of scientific literature about how related the two organisms are, and the best estimate for when they diverged. One of those papers might have a % similarity, but really all the other stuff is the interesting part.

To add to @WYSIWYG's comment, genome-wide DNA similarity is not much studied. The part that would be somewhat interesting (a rigorous full-length nucleotide-for-nucleotide comparison) is computationally and technically extremely difficult if not impossible today, and the methods that have been used in the past to get the numbers you see are both technically difficult and scientifically uninteresting. You might find mitochondrial similarity, or similarity over a few genes, but you are unlikely to find an actual answer to your question, except in general terms.


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Mechanism to limit the exponential growth of the number of ancestors that are n-generations away from an organism?
The context is organisms with sexual reproduction, with 2 parents per organism.
Construct the family tree of one such organism, back into geologic time.
Take a(n) as being the number of ancestors that are n generations distant.
The function a(n) has an exponential character (at least in the beginning, with n sufficiently small).
For 2^n, simple math gives:

After 20 generations, you have about 10^6 ancestors.
After 30 generations, you have about 10^9 ancestors.
After 50 generations, you have about 10^15 ancestors.
After 1000 generations, you have about 10^300 ancestors.

I've read one estimate that there are about 10^80 atoms in the Universe. What does this mean?
It's important to note the the members of generation n usually aren't all alive at the same time.
As an example, for humans, the birth-dates of generation-20 are roughly between the years 1720-1520, for example.
It doesn't take very many generations for a(n) to exceed p(t), the population as a function of time.
This is accounted for (at least for sufficiently low n) by the fact that a(n) represents organisms that aren't alive simultaneously, while p(t) does.
I understand that.
But, this effect, important as it is, seems to be linear with time.
As such, it doesn't seem capable of limiting the exponential growth of a(n).
In this context, inbreeding is often raised.
But, in my opinion, inbreeding is not germane.
Here, all that matters is that each organism has 2 parents.
Period.
Whether or not inbreeding was involved doesn't change that basic fact.
All inbreeding means is that one ancestor is a member of more than 1 generation.
That's not relevant to my question.
Edit later:
No, inbreeding is germane. It means that 2 members of a(n) can have the same two parents in a(n+1). That reduces the exponential growth of a(n).
It seems that a(n) must be limited by something, for sufficiently large n. What is that something?

In addition to @mgkrebbs answer, note that "inbreeding" refers to breeding among closely related individuals. Individuals several generations removed are not closely related.

Of course a(n) is limited, and much more tightly than by the number of atoms that exist.  The analysis in the question goes off track with "inbreeding is not germane. Here, all that matters is that each organism has 2 parents. Period."
Consider a person whose parents are first cousins. Then:

a(1) = 2
a(2) = 4
a(3) = 6, not 8

While each of the two parents has four grandparents, together the two parents have only six grandparents because they share one pair of grandparents.  This is due to pedigree collapse.
This table shows the actual collapse for some people with ancestry known to nine generations and with significant inbreeding (from de.Wikipedia):

I just realized that it's germane. I have edited the question a second ago. So is inbreeding the only mechanism for limiting the exponential growth of a(n)?

I see. It's this pedigree collapse idea which is the key. Thanks!

@JohnO at a point all organisms are a product of inbreeding since we all evolved from the same LUCA.


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Why is synthesis of tetanospasmin advantageous to C. tetani?
The tetanospasmin is a neurotoxin synthesised by some strains of C. tetani. It is the factor causing tetanus, but what is its role for the bacteria itself?
I do not believe the main objective of C. tetani is to harm people. I believe that any organism that wastes resources for purposes not related to its reproduction or preservation is being wiped out by the evolution.
As tetanospasmin is encoded by a plasmid gene, it should be pretty easy ro get rid of and there are strains of C. tetani lacking the gene. As protein synthesis costs resourcess, I guess there is some advantage from the neurotoxin synthesis - otherwise it would be a searious handicap, leading to competitive exclusion of tetanospasmin positive strains.

It's an opportunistic and generalist bacterium, existing in soil, digestive systems it's probably everywhere. It's related to Clostridium botulinum which ialso makes one of the most powerful toxins know, and the two may have similar ecology and purpose. I know botulin can in bee honey enough for old honey to be dangerous to babies, which gives an idea of habitats. There's some info on tetani ecology on the web, i don't know precisely. The toxins it produces may be harmful to humans as a side effect of it's more common habitat where it needs to establish an ecosystem and defend itself.

This paper suggests that botulin, from a close cousin bacteria of tetani, has an unkown mode of evolution: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357194/

@LifeInTheTrees Bee honey doesn't contain the toxin otherwise it would be harmful to adults as well. Bee honey contains spores of clostridium. Clostridium can take over the gastrointestinal flora of babies as long as they haven't set up sufficient beneficial germs. Then the clostridium germs can produce the toxin inside the babie's bodies.


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Fluorescence assays to identify protein concentration without adding a large peptide sequence?
I'm trying to find a way of tagging a protein with something visually quantifiable to track protein concentration through potential purification steps and screen for the most efficient such steps. However, GFP and its cousins are very large proteins that would change the properties I'm targeting for purification, making them non-starters.
Is there a tag that through fluorescence, colorimetrics, etc. can be used to quantify concentration of a single protein while minimally altering chemical/physical properties of the protein for purification?

It is difficult. There are "click chemistry" tools but you would need to find a way to make some modifications on the desired protein in vivo.

Are small tags an option (FLAG-tag, HA-tag, Myc-tag)?

@Dr.H.Lecter the tags by themselves are insufficient. You would need an antibody to mark the protein.

Indeed, but you can generate a fusion protein much faster than creating an specific antibody from scratch. Besides antibodies against the tags I mentionned are commercially available and easy to get.


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What are the coverings of femoral hernia?
It was my Viva question and I was really puzzled.I know what is femoral hernia and it route like the abdominal content moves down the femoral canal and further through the saphenous opening and all but I have no idea about it's coverings.Can anyone please help me

Femoral hernia coverings (from inside out):

Peritoneum
Femoral septum (extraperitoneal fatty, connective and lymphoid tissue)
Tranversalis fascia
Cribriform fascia
Superficial fascia
Skin

Image source: SurgWiki, Creative Commons Licence
Sources:

SurgWiki: Hernias
SlideShare: Femoral hernia, p. 12
EarthsLab: Femoral canal
Textbook of Anatomy Abdomen and Lower Limb;, Volume 2, By Vishram Singh, p.45


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Is sexual desire stronger in men than women?
Usually in popular culture it's considered men sexual desire is stronger than women. This seems to be congruent with the availability of sexual related items for men and women, such as magazines, movies, and more. Trying to understand if there is a biological connection to this, I found these paragraphs in some articles.

Estrogen, progesterone, and testosterone are hormones that affect a
  woman’s sexual desire and functioning.
When it comes to sexual desire, the most influential hormone is
  testosterone. Though it’s often considered a male hormone,
  testosterone — like estrogen– is present in both men and women, though
  the proportions differ between the sexes.

Hormones affecting sexual desire
and

On average, in adult males, levels of testosterone are about 7 to 8
  times as great as in adult females.[7] As the metabolism of
  testosterone in males is more pronounced, the daily production is
  about 20 times greater in men

Testoterone
Is this greater production of testoterone in men related to a stronger sexual desire? Is there any research studying this, or studying differences between male and women sexual desire intensity in general?

Some of the work of Bob Trivers makes some sense to me. He talks about parental investment https://en.wikipedia.org/wiki/Parental_investment.
The "investment" of a man could be as little as paying for dinner, followed by a few minutes of sexual pleasure, and then he is free to go. The woman's investment for the same thing is the risk of pregnancy (or cryptic STD). Pregnancy is difficult, and before modern medicine, was one of the most common ways to die for women. Then she must feed a helpless infant with her own body, and tend to its needs for the next 15 years. We have social structures for the man to stick around and contribute. But these are not biological differences. The man can leave. The woman cannot. She bears virtually all the risks of sexual behavior. Of course, sexual desires vary by individuals, likely in a bell-curve that overlaps (I anticipate some PC doofus pointing out that some women have strong desires, and some men don't). But I would not be surprised at all, given the biological differences in risks and investments between men and women, that the peak of these overlapping distributions is higher for men than women. Also, evolutionary fitness is defined by the number of offspring an individual can produce. A man's strategy is fundamentally different than a woman's. A man who has 1000 sexual partners is likely to leave more surviving offspring than a man who marries the woman he loves, and stays faithful. A woman with 1000 sexual partners would not be able to have hundreds of children, and would likely put her health at risk.

You are saying as if the only result of sex pertinent to evolution is getting pregnant or an STD. Women have menstrual cycles with concealed ovulation which allows them to be sexually active almost all the time. They can have sex during pregnancy. These kinds of non-reproductive sex can help to keep the man around and have more resources and better-protected children. So women may have evolved to have less desire for new partners but not lower overall sex drive. Or not. It just hard to reason without actually measuring it.

I did not say that this was the only explanation, but it seems to fit many observations across a wide range of animals. Yes, hard to measure. However, what do your observations tell you? How common do husbands complain that their wives want "it" too often, relative to the other way around?


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what's the difference between traditional genetic engineering and and CRISPR?
While at school, I learnt about restriction enzymes and how you could insert foreign DNA into an organism.
When I first heard about CRISPR I thought it was very similar except much more precise/targeted.
It seems however that CRISPR only allows editing (substituting nucleotides)
What are the differences, advantages, etc?

In what organism? In yeast for example you don't need restriction enzymes nor CRISPR for precise engineering only PCR products.

Bacteria and archaea evolved CRISPR as part of their adaptive immune system to protect themselves from invading viruses and foreign plasmids. The defence system relies on small, non-coding RNA molecules (CRISPR RNAs/guide RNA) that in association with a CRISPR associated (Cas) protein silence foreign sequences by means of cleavage. Twenty nucleotides at the 5’ end of the CRISPR RNA, corresponding to the protospacer region, direct the Cas9 protein to a specific sequence within the DNA using predictable Watson and Crick base pairing between the target DNA and the guide RNA, triggering enzymatic cleavage of the foreign DNA. Essential for cleavage is the presence of a sequence motif immediately downstream of the target region, known as the protospacer-adjacent motif (PAM),the PAM sequence in S. pyogenes (the most widely used system) is NGG. Because a sequence match also exists between the guide RNA and the host’s DNA that encodes it, it is vital that the guide RNA identifies bona fide targets without attacking the host chromosome. Discrimination between the target and host protospacer is achieved by the Cas effector recognition of a PAM sequence that initiates binding and cleavage of the foreign DNA. Changing the DNA target site that is specified by the 20 nucleotides at the 5’ end of the guide RNA redirects the system to target a different DNA sequence, making it a highly versatile and programmable tool. In 2012, the CRISPR system was  programmed to cleave specific DNA sites in vitro and since then, the system has been widely used in many gene modification applications.
CRISPR allow so much more than just substituting nucletodies. Like you say, CRISPR is a much more precise system than restriction enzymes, the guide RNA for CRISPR systems is typically around 20 nucleotides long so it can theoretically be used to target a unique site in the genome (4^20 = 10^12, so only the recognition site is expected to feature once 1 in 10^12 bases, N.B. the human genome is only 3x10^9 base pairs in size).
There are several options using the CRISPR with an active Cas9 protein, the first is to create a gene knockout, which removes the function of a gene. Gene knockouts can be performed by targeting the CRISPR-Cas9 system to the start of the gene and cleaving both strands of the DNA to generate a double stranded break which will be repaired most likely by the cellular repair pathway non homologous end joining (NHEJ). NHEJ results in insertions or deletions and so will most likely result in a frameshift mutation which alters a large amount of the amino acid sequence in the gene or introduces an early stop codon, so the protein produced is non functional. Alternatively a conserved residue (e.g. a catalytically important residue) in the protein can be targeted and mutation of this can remove the catalytic function or recognition domain in an enzyme or protein. NHEJ can also be used to mutate DNA that codes for RNA products. Additionally, the CRISPR system can be targeted to regions outside of the coding sequence such as the promoter or enhancers and silencers/operators (depending on whether prokaryotic or eukaryotic), which can also remove the functionality of the gene.
The CRISPR system can also be introduced to the cell  together with a single-stranded or double-stranded DNA template to make very small and precise changes to the DNA (e.g. single base mutations), or insert DNA sequences up to thousands of bases in length so that entire genes can be incorporated into the target region. This more precise editing method also involves the double stranded break formation by the cas9 protein, but relies on different cellular repair pathways: homology directed repair, the most common form of which is homologous recombination. Importantly, the template DNA must have homologous sequences to the DNA flanking either side of the double stranded break. In the presence of the correct exogenous DNA template, homology directed repair can occur in which the exogenous template DNA is incorporated into the target DNA in exchange for the damaged DNA.
Other use of CRIPSR include using a catalytically inactive cas9 protein (dead Cas9). This system is unable to cleave DNA, but is still able to target specific sites in the DNA. dead Cas9 can be fused to or recruit effector proteins for regulating gene expression at the transcriptional level, as well as guiding enzymes capable of precise base editing without introducing double stranded breaks. The dead cas9 system can be fused to transcription repressor domains such as the Krüppel-associated box (KRAB) or transcriptional acitvators such as VP64 for effective and specific repression or activation of gene expression at sites that don't contain recongion sequences for these effectors. dead Cas9 can also be used to recruit epigenetic modifitying enzymes such as methylases and acetylases to regulate gene expression this way. Additionally, this system can be fused to DNA base editors, which are enzymes created by directed evolution that are capable of causing efficient and specific point mutations in DNA and RNA (this is much more specific and effective than point mutations using homology directed repair), although RNA editing required using cas13.
Gene editing can be used to repair disease causing mutations, introduce new genes with novel functions into organisms' genomes, transiently alter gene expression to treat diseases; create knockout, knockdown and knock in strains for studying the effects of genetic factors on phenotype and even more.
In contrast, restriction enzymes typically have recognition site of 6 nucleotides and so they will cut at many orders of magnitude more sites than CRISPR will (4^6 = 4096, so 1 in 4096 nucleotides are expected to be a cut site for restriction enzymes) so they are not suitable for specific editing of genomes as they will cause non specific fragmentation of genomic DNA, which will kill the organism, so CRISPR is a much better enzyme for editing genomes. Instead, restriction enzymes are used in molecular cloning to generate sticky overhangs (or blunt ends) for the assembly of DNA molecules to generate recombinant DNA.
Although the PAM appears to limit the number of target sites that the CRISPR system can be targeted to (around 1 in every 16), through directed evolution, a Cas9 variant with increased PAM compatibility has been developed. This new Cas9 is capable of recognizing PAM sequences including NG, GAA, and GAT, this makes it  more versatile and greatly expands the number of targets available for site-sensitive genome editing applications.
Whilst CRISPR based gene editing is very exciting, a lot of work is still needed to: increase the specificity of the system as it causes numerous off site mutations, which can be lethal to cells; to increase the effectiveness of delivery of the system in vivo to large organisms such as humans; to reduce the immunogenicity of the system (it can trigger an immune response in humans) so that it is safe to use; as well as increase our understanding of the affect of making specific mutations in humans (e.g. which mutations can treat diseases safely).
References/further reading:
Jinek, M. et al. A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science (80-. ). 337, 816–821 (2012).
Repurposing CRISPR as an RNA-Guided Platform for Sequence-Specific Control of Gene Expression. Cell 152, 1173–1183 (2013).
Liu, X. S. et al. Editing DNA Methylation in the Mammalian Genome. Cell 167, 233–247.e17 (2016).
Zalatan, J. G. et al. Engineering complex synthetic transcriptional programs with CRISPR RNA scaffolds. Cell 160, 339–50 (2015).
Hu, J. H. et al. Evolved Cas9 variants with broad PAM compatibility and high DNA specificity. Nature (2018). doi:10.1038/nature26155
Cox, D. B. T. et al. RNA editing with CRISPR-Cas13. Science (80-. ). 358, 1019–1027 (2017).

so use of CRISR is limited by the presence of PAM sequence in the target DNA?I mean say Cas9 recognize NGG,so I can only edit the sequence near to NGG?

I left that out at the time because there has been a lot of work done to reduce the requirement of Cas9 proteins for recognising a PAM sequence, but I have edited the answer to include a note on it.

As a note about this: "increase the specificity of the system as it causes numerous off site mutations", J. Doudna and E. Charpentier both said that CRISPR-Cas9 was very specific and that was far from the major concern at that point. Also discussed here: https://biology.stackexchange.com/questions/49106/how-specific-are-crispr-cas9-cuts

I would strongly disagree with you, there has been masses of evidence showing that CRISPR is not yet specific enough for targeted therapeutic applications:https://science.sciencemag.org/content/364/6437/289
"The technology requires further development to limit off-target editing." A quote from a paper written by Jennifer Doudna - DOI: 10.1126/science.aat5011.
Look at the recent mess up with gene editing cows, the technology is far from where we want it to be in terms of specificity - https://www.technologyreview.com/s/614235/recombinetics-gene-edited-hornless-cattle-major-dna-screwup/

CRISPR is a gene system used by bacteria to resist virus invasion/avoid mammalian immune response. Scientists use RNA to guide cas9 nuclease to cut and modify specific genomic sites in a variety of cells, including IPS. The Rudolf jaenisch team injected cas9, te1 and tet2 specific sgRNA into the fertilized eggs of mice, and successfully obtained the homozygous mice with double gene knockout, with the efficiency up to 80%. They co injected cas9/sgRNA with primers with mutated sequences, which can accurately introduce the required point mutations into two genes of mice. In ES cells, they successfully knock out five genes at a time. Compared with ZFN/talen, CRISPR/Cas is easier to operate, more efficient, and easier to obtain homozygous mutants, and can introduce multiple mutations at different sites at the same time. But whether the system has Miss target effect needs further study.
The traditional transgenic and gene targeting technology, due to its stable and mature technology, can modify the genome sequence of mice and rats, and will still be the main technology of model animal construction. If ZFN/talen, especially CRISPR/Cas, can solve the Miss effect, it may be widely used in the preparation and research of mice, rats and other model animals, and become an important supplement to the traditional transgenic and gene targeting technology.

Welcome to Biology.SE! It isn't clear that this adds anything to the very thorough existing answer and seems to incorrectly imply that CRISPR isn't already widely used. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


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Cleaning Masterclave
When i finish operation. My masterclave has smell, I think has media moulecular bind into the surface and microbial can live in. My labs don't have SOP to clean it. I promote use detergent but wonder it'll bad effect in the suface. Do you know how I can clean masterclave effective?

This's my masterclave

Have you contacted the manufacturer?

Sorry, my mistake. I don't think it. I will contact manufacturer.


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Is there any organism that is born with all the nutrients and resources needed for their entire lifetime?
I understand that adult mayflies have no mouth, but they do take in oxygen through openings in their exoskeleton.
Is there any organism that does not need to ingest any type of nutrition and does not need to take in something for cellular respiration?

Assuming you don't mean an immortal organism, do you mean a type of organism (species) that can reproduce an equivalent offspring organism without inputs?  How could that work, since without inputs the offspring would have to be smaller than the parent (and thus not equivalent)?

@mgkrebbs I'm not familiar with an immortal organism in a biological context.  Yes, I mean a species that can reproduce an equivalent offspring organism.  I wouldn't imagine that would work.  It came up in a discussion making a comparison of biological life with the claim there is a non-biological system that is alive.

You may need to clarify your question: As written, this would be the biological equivalent of a perpetual motion machine. No such organism could reproduce without either violating the first and second laws of thermodynamics, or ultimately evaporating into nothingness as it divides.

Well that answers my question.  There are no such organisms.

No, I think this fails even on simply definitional terms.  That is, Life is (sometimes) defined as meeting certain criteria, such exhibiting growth, metabolism, and response to stimuli.  Those will all require intake of some external substance at some point.
To get even more pedantic, all cells have a cell membrane, which is selectively permeable to certain molecules.  Every organism will thus passively let in some substances from the environment, and thereby failing your criteria.

Luna moth , so I expect there are other moths.

Luna moth caterpillars do feed.

The adult moths do not eat , per Wikipedia.

You are correct that adults don't eat, but the question was about organisms being born with all their lifetime nutrients. I would argue that a caterpillar eating means that luna months are not born with all their required nutrients.

I would point that maybe there is an organism that can pass enough nutrients to 1 generation to survive and reproduce, but not continuously generation after generation.
Search in this camp, you may find something.


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What is this hard shelled insect in my house?
I moved to a new city in west India last year and I've since, on several occasions, seen this insect on walls and it's usually climbing using its head. It has a greyish long shell and moves in a very wobbly way. I've asked people in the locality if they know what that insect is, but no one has a clue. And my curiosity is piqued everytime I see it and I really want to know what it is.
Here are two closeup images:
https://ibb.co/HNDLCMm
https://ibb.co/6JCMH7j
I have a video as well but I don't know how to share it here.
I was suggested that this question is a possible duplicate of: What insect is this? (India)
The insect in my case is probably much smaller and has a plain grey shell (as opposed to building a shell from material lying around, which would most probably be different every time). I don't explicitly see any legs although there may be.
I want a definitive answer as to what moth it is or if it is one or not.

Possible duplicate of What insect is this? (India)

I think if you want a better ID you need a much much better picture.

Your close-up images are not any better than the current one.

Related: Identifying a creature that appears to be a worm wrapped in a cocoon, What is this black and white worm in a white case?,  Help in identifying an unknown arthropod, What insect is this? (India), Identify this smooth-cocoon worm from Southern India, Small worm living in some kind of cocoon......

Related:  What is this animal that hides in dustlike structure?, What in the world is this critter?, What is this hard shelled insect in my house?, What is this insect found commonly in coastal India?, Insect identification - pantry moth vs clothes moth

That's a plaster bagworm [ https://en.m.wikipedia.org/wiki/Phereoeca_uterella ] :)

Doubt if it's the same species. Probably a different one since it's always grey (but could be that the larvae are rising from same source and using the same material). It is a moth larva for sure though right?

For sure it's a moth larva because it's order is Lepidoptera.. and lepidopterans are either butterflies or moths.


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

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

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


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Where does the number 67 in the nuclear protein/antigen Ki-67 come from? Why not 66 or 68?
I have read in in the original paper that in the year 1983 a research group in Kiel, Germany (that's where the Ki- in the name comes from) developed monoclonal mouse antibodies against Hodgkin lymphoma cells in multiple 24-well plates. If I understand correctly they were able to isolate antibodies from 63 wells and divided them into 493 microtiters into several 96-well microtitre plates. Of these 493 titres, 164 cell batches were chosen for further investigation and expanded. Somehow Ki-67 emerged from there, but why this number? Who gave it that name and why?
A teacher once told us in med school, the cells producing the antibodies were found in well 67, but I cannot find any source to back up that claim.

There's this article, but who knows where these authors got the idea from...

From Wikipedia: "The name is derived from the city of origin (Kiel, Germany) and the number of the original clone in the 96-well plate".

That statement in the wikipedia article is unsourced ...

Yes that's the legend, but I want details...


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Are any genes over a billion years old?
Are there any genes (for any organism) for which we can say with confidence that they are over a billion years old?

Ribosomal RNA (rRNA) genes are shared among all living organisms, including lineages that have diverged from one-another well before a billion years. Bacteria, Archaea, and Eukaryotes diverged over 3 billion years ago, and their rRNAs are virtually identical to one-another. http://www.biologyreference.com/Ar-Bi/Archaea.html
Any genes that are shared between plants, animals and fungi would also be over a billion years old.

"…their rRNAs are virtually identical to one-another." No. Just counting the bases, typical examples are ssRNA: bacteria 1542 nt, eukaryotes 1869 nt; lsRNA: bacteria 2906 nt, eukaryotes 5070 nt. They are certainly related, but a nuanced explanation of how is required. See e.g. R. Brimacombe (1984) TIBS  9  273–277.

Counting the bases is meaningless. Eukaryotes possess non-conserved expansion segments that account for virtually all the variations in length. You can take ribosomes from a prokaryote, and insert them into eukaryotes, and they still function. I stand by the fact that they are virtually identical. Saying that they are related is obvious, but seems to indicate a lack of understanding for how genes evolve following their divergence after speciation. At the time lineages split, the genes are identical. Then the nucleotides change over time, but the structure remains.

I didn't want to answer myself and inevitably overlap with yours, so I suggested you edit it to clarify the point. But I have no wish to argue the point, I'll just write one of my own when I have the time.


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Which trait does the given Pedigree chart show?
I have a doubt in this pedigree chart , according to me it should be autosomal dominant. But the ans given is X linked recessive , in the case of X linked recessive one daughter should be carrier and not affected , but in the chart it's shown the daughter is affected and not a carrier .
What should be  genotype of female parent ?

Please do not post questions as photos of text. It discriminates against people using screen readers and cannot be indexed.


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What would be the effect of excess taq polymerase on the PCR?
I just had one question regarding the possible effect of putting to much Taq polymerase in my PCR tube?
Instead of 5µl I put 50µl (10x more).
Do you think it will have a bad effect on the reaction??
Thank for your help.

I'm voting to close this question as off-topic because it is a question of no general interest to the Biology community, which is what this site is trying to accumulate.

@David, I think it is valid question for newcomers.

Costly error.
And yes, it will affect your reaction, since the concentration of Magnesium ions, which are needed as a co-factor by the enzyme, is too low. If you need so much PCR product, you can now adjust the rest of the reagents or you could start over and put this on your personal list of errors. Always check the amount of volume, if it is suspiciously high, check again.
If you decide to proceed and work with a 10x larger volume, make sure that the single PCR reaction is not bigger than 50µl, because the bigger volume also affects how fast the reaction heats up and cools down. If your reaction is too slow to reach 72°C for example, the elongation time might not be long enough to get the full product. If denaturating is too short, your efficiency will drop.

Thank you very much for all these explanations.


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Why is sickle cell trait expressed in half of all cells rather than all cells containing half-sickled haemoglobin
If sickle cell trait is due to be heterozygous with respect to a single gene mutation on the haemoglobin β-globin chain, why is it the case that ~50% of RBCs are sickled rather than half of the haemoglobin in every RBC containing haemoglobin-S β-globin chains?
Is it due to some form of monoalleic expression that occurs by chance or are all the proteins in one RBC formed from one random allele during erythropoiesis?

Welcome to SE Biology. I am not sure that I understand what you say or that it is correct.  What do you mean by the "trait  is due to be heterozygous"? The heterozygotes are carriers and do not suffer sickling. Only the red cells of homozygotes sickle. Likewise your statement about only half the blood cells sickling. Presumably that is just statistical chance as the oxygen concentration decreases and nothing to do with expression. Could you please clarify and support your statements with links to references. Then we may be able to help sort it out for you.

Sickle cell carriers (heterozygous) don't have sickle cells, but do have altered blood cells

"The sickle cell trait" affects people who are homozygous for the HbS allele. These individuals only have hemoglobin S (after all fetal and embryonic hemoglobin genes are switched off). Hemoglobin S forms large crystal aggregates under conditions of low oxygen tension, and cause red cells to sickling and then to lyse. Anemia is most often severe and lethal.
Heterozygous subjects (HbA/HbS) form both hemoglobin A (normal) and hemoglobin S in approximately equal quantities, and suffer only a mild form of anemia, that may be even unnoticed.


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Found this spider in my garden
I found this guy in my backyard. I have no clue what he is, though I'm assuming it's a jumping spider after doing a little bit of searching.
For context, I live in Southern California, close to being right in between LA and San Diego. It's suburban, though there are a few reserves that are close by. It is incredibly small, probably no bigger than a dime. It's mostly orange and black with some rings of white on the legs. It's pretty hairy as well.
The only thing I'd like to know is if it's poisonous or dangerous, as I don't need my dogs getting sick or injured. If possible, I would also like some links for some background reading on it!

All spiders are venomous. This is a jumping spider, family Salticidae. https://en.wikipedia.org/wiki/Jumping_spider. I am not sure of the species, but they are not "poisonous" (if you mean dangerous to people). They are diurnal hunters, and they may bite if harassed. But the bite is not harmful, unless you are a bug.

As Karl mentioned in his comment, this is a jumping spider in the family Salticidae.
Based on your location and the coloration, I would suppose this might be Phidippus adumbratus.

 Source: Wikimedia
You can see more pictures here and here.
I don't think the angle nor zoom quality of your photo can be used to definitively ID your specimen to species. However, as you can see in the photo above, P. adumbratus is not a bad candidate.
According to Edwards (2004) this genus is sometimes difficult to tell apart, but P. adumbratus can be distinguished from other Phidippus species as follows:

Males can be distinguished from the closely related P. boei (and all other species of Phidippus in California except P. aureus) by the orange scales dorsally on both carapace and abdomen (P. boei is black with a red abdomen dorsally), although island populations have the OQ scales darker and reduced in number. P. adumbratus has a much longer, narrower embolus apical portion than P. aureus. Females can be distinguished from P. kastoni by the shape of the internal ducts of the epigynum; the duct heads are narrow in P. adumbratus (broad in P. kastoni) and the gland is visible as a rounded projection on the anterodorsal surface of the duct head (not visible in P. kastoni). Females are covered dorsally with orange or gray scales (usually with white abdominal spots), unlike the females of P. boei, which have a similar epigynum but are black in color without markings, or with red dorsal scales only on the abdomen (without spots).

If you'd like a much more detailed of description of P. adumbratus (or others in this genus), you can find whole-page detailed descriptions in Edwards's publication quoted and linked above.

A map of geo-referenced records from GBIF shows the occurrence of this species in southern California:

Edwards, G.B., 2004. Revision of the jumping spiders of the genus Phidippus. Occasional Papers of the Florida State Collection of Arthropods, 11.

@Clouds please kindly mark this as an accepted answer if it is satisfactory or describe any concerns you have with my answer. Thanks!


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Enzymes extracted from diferent tissue, may have diferent $K_m$ values under the same conditions?
My laboratory team has been used succinate dehydrogenase (1.3.5.1) from Gallus gallus domesticus breast (the most meated part of the chicken, where you will obtain nuggets) to determine $K_{m}$ and $V_{max}$ under 3 linearization methods.
But, in BRENDA page, I found various values for many organisms, like Bos taurus, and they select other tissues like liver tissue.
Why the difference?
PD. Any reference about where to find this values for Gallus gallus mesticus will be very appreciated.
EDIT: The reaction consists on dehydrogenating succinate to fumarate, on the tricarborxilic acid cycle. Include the creation of a trans-double bond.
Describing my laboratory practice, we macerate the meat with glass sand, and divide this mixture on 2 kinds: one with methylene blue and trichloroacetic acid (TCA) and one without TCA. Now I know that TCA is a protein precipitant, and methylene blue is an indicator; the less blue, the less succinate. So, with absorbance tests, we can elucidate [Succinate] vs time plot, and approximate the ratio $V_{max}/K_m$ from the michaelian equation for substrate concentration decay:
$$S(t)=S_0 e^{-\frac{V_{max}}{K_m}t}$$
Also, i think it will be possible modeling instantaneous velocity with its derivate and make the linealization plots, but i'm not very sure of this.
EDIT2: Thanks for the help with my practice report (I really appreciate it), but I still wanna know if it's possible to have different $K_m$ values on the same enzyme, only changing the tissue for reaction.

Can you please [edit] your question to add an example of such enzymes from BRENDA?

Also note that succinate dehydrogenase is a part of a complex and catalyzes many coupled reactions. A simple MM kinetic model won't apply in this case, I believe. Which reaction are you interested in?

As far as I know Brenda lists experimentally determined values, if they come from different studies/sources the differences are much more likely to be due to that than due to different tissues

I need experimentally values reported, so data in BRENDA is usefull. But I duno why it will be different values on different tissues. This is not possible, under the same conditions?

user1136 thank, I didn't know about the protein precipitation effect of TCA. That changes everything, since the Rx have a non-competitive inhibition.

user1136 In fact, I didn't found different values for $V_{max}$, I found different values only for $K_{m}$ and the ratio. If you know a website or a book where I will found it, can you tell me, please?

My teacher derived that formule from Michaelis-menten eqn assuming that $K_m >> S_0$ and omitting it at denominator. Then: $$V_0=\frac{Vmax . S_0}{Km} = -\frac{dS_0}{dt}$$ but this is not my question. Maybe I need to open another question for linealization?

I'd like to do that. That was i'm thinking. But my partners, who have re-coursed enzymology, used another method using an equation that I don't even know. If you are interested, i let you the link to the report, but is in spanish and i can't explain it to you at all. [  https://1drv.ms/w/s!AtNW_8yW8ySxgkGDfKg4KoHaWzbp ] You know, mathematics don't have a language. They are a language.

You would not expect the same enzyme from different tissues to have different Km values if the enzymes are truly identical.
In addition, you would not expect the Km value to change during purification: the Michaelis constant for the purified enzyme should be the same as that determined with a crude sample.  If this is not true, it might mean that the enzyme has become modified during purification, perhaps by proteolysis (not something you want your examiner to point out or suggest!).
One advantage of the Michaelis constant is that it is independent of enzyme concentration (and so does not depend on the degree of purity).
Having said that, I think it would not be considered too unusual for enzymes isolated from different tissues to have different Km values.
Possible reasons are:

The assay conditions are not really the same. pH, ionic strength, temperature and buffer composition may all affect  Km.  The Michaelis constant determined at pH 7 in 100mM phosphate at 37oC may be very different from that determined in 50mM Tris pH 7 and 25oC
Post-translation modification may be important.  The enzyme from one tissue may be phosphorylated, for example. One laboratory may have isolated the modified from, whereas another laboratory may routinely include phosphatase inhibitors.
Proteases present in the crude tissue preparation may have modified the enzyme.

In the case of succinate dehydrogenase, there are two other important considerations.

Succinate dehydrogenase is a membrane-bound enzyme (containing a covalently bound flavin) and the method of extraction will be all-important, and a key area to examine is whether extraction conditions may account for the difference in Km.
Finally, and this one is important I think.  SDH is a two-substrate enzyme and the Km for substrate A will depend on the concentration of substrate B ! To determine the 'true' Michaelis constant for a two-substrate enzyme (assuming no substrate inhibition), we must extrapolate to 'infinite' concentrations of the co-substrate. Otherwise we are dealing with apparent Km values.

I'll bet the last point is important. Is the problem that at least some of the reported Kms are apparent values, ie the concentration of co-substrate is different under the different experimental conditions?

One advantage of the Michaelis constant is that it is independent of enzyme concentration (and so does not depend on the degree of purity).   This is strictly true in the limit of dilute enzyme concentrations and saturating substrate concentrations, $[S]{tot} >>[E]{tot}$ which is usually the case but not necessarily feasible at all stages of purification. If Km is determined in subsaturating conditions (or concentrations that cause protein aggregation) it will apparently change over the purification.

"... which is usually the case but not necessarily feasible at all stages of purification" ?? In my experience,  [S]o will always exceed [E]o at all stages of purification This is one of the simplifying assumptions of the steady-state approximation, under which Km is usually defined. Can you give an example where this is not feasible during purification. (ii)  "If Km is determined in subsaturating conditions" Subsaturating concs of what? Of [S]o ?  This has to be the case if a rate is determined at sub-Km concentrations.  Of [E]o?? But the usual assumption is that Eo << So (always)

Can you give an example where this is not feasible during purification.  If the substrate has low solubilities (for example, gualylates, methyxanthines) then at high enzyme activities the maximum feasible substrate concentration can be subsaturating. If the enzyme has a high specific activity, for example superoxide dismutase, then obtaining saturating substrate concentrations can also be difficult. There are some obvious technical solutions to these problems but, if they aren't implemented correctly, the apparent Km will change over the purification.

If the substrate has a low solubility it may be impossible to determine the Michaelis constant at all stages of purification if the highest conc of substrate that can be obtained in the assay is way below Km. But this does not mean that the Km has changed during purification.  As long as assay conditions differ only in the degree of purity of the enzyme, and as long as the steady-state approximation applies, one would not expect the Michaelis constant to change during purification.  The purified enzyme will be typically diluted to ensure steady-state conditions, for example

i didn't say Km actually changed I said it can apparently change over a purification.

A Km can change over the course of  a purification. Solubilization of a membrane-bound enzyme could change the Km, as could proteolysis. I have made this point.  This is an undesirable (but perhaps unavoidable) outcome as the enzyme is no longer in the 'native' state. But if the Km is determined under steady-state conditions there is no problem whatsoever in determining a Km with a crude sample, as Km is independent of enzyme concentration (under SS conditions). This is what allows us to compare.  Most of the early work on enzyme kinetics, for example, was done with impure preparations.


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Which insect is this? They crawl like caterpillars and get metamorphed into orange moths
 They are like larvae which gets metamorphed into moth (orange colour with black spots) .They are multiplying rapidly and have spread all over our building.

Resembles wooly bear caterpillars while the moth you shown is very identical to black-banded orange moth (Epelis truncataria).


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What is autophagy?
Recently Japanese scientist won Nobel Prize in Medicine for "Autophagy".
Can someone explain what autophagy is?
https://www.google.com/amp/s/www.livescience.com/amp/56349-japanese-scientist-wins-nobel-prize-in-medicine.html

I'm voting to close this question as off-topic because questions about diet and nutrition are off topic unless directly related to medical care.

@CareyGregory I've edited the question. Is it valid for the site now?

You fixed the nutrition problem but asking how this will benefit people is purely speculative, and therefore opinion. So I edited your question down to the root question you're asking and reopened it. People can add their thoughts on what it might lead to in their answers, but get the basic question answered first.

Welcome, @Saksham, I've closed your question as a duplicate because I think a Q&A here already answers your question. This isn't any sort of punishment, it's just the way SE is meant to streamline questions. If you have further questions that are not answered in the marked duplicate you can ask a new one. Thanks!


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Why are children so violent, compared to other adolescent animals, when they play?
When children play it is frequent that someone starts crying, suffers minor injuries and that they are intentionally mean towards each other (e.g., bite, pull hair, throws sand, pushes someone so they fall, wrestles so hard that the weaker part struggles with breathing and so on). On the other hand, when my puppies (or even adult dogs) play you never see anything like that. They tumble around and takes turns for who's on top. The only "negative" I have ever seen is when puppies with "flappy" ears play and someone gets hold of an ear with their sharp teeth - then the "victim" might scream, but when this happens the other dog immediately let go of its grip.
Children that play need parental supervision. Young animals that play manage fine without their parents.
Why are humans so cruel when they play compared to other animals?
(I'm not sure if this belongs biology, pets, psychology - if I picked the wrong site, please move the question to where it belongs)

I personally have seen dogs run whimpering and bloody back to their owner after play with another dog at a dog park went off the rails. I suspect your observation is just your observation, not a hard rule of animal behavior.

@CharlesE.Grant Dogs can get into fights but that is not playing. Cats frequently fight, which most cat owners that let their cats out are aware of.

I’m sure it doesn’t belong here. Can you envisage a definitive objective answer?

@David Yes, something with the evolution.

So somebody says "things evolved that way because…" and that is regarded as a definitive objective answer. If I see amino acid sequences I can see evidence for evolutionary propositions. When I read incantations of the former sort — always presuposing the answer — it reminds me of when people would invoke  God in replies.

@David If it can be falsified in line with Popper's ideas about critical rationalism it is an acceptable answer.

I am skeptical of every part of this -- that human play is necessarily violent or that animal play is different. Certainly in my own kids and their cohorts, "wrestles so hard that the weaker part struggles with breathing" would be appalling and highly unusual. Dogs are tamed animals; is play among young wolves non-violent? What about chimpanzees or baboons?

@RaghuParthasarathy Do your kids never form "a pile" with someone at the bottom having a bunch of kids on top making it hard to breathe? Maybe it requires a school class or something but with enough people around, the kid at the bottom might struggle.

I believe wolf puppies play friendly yes. They might fight over food but when playing I have never heard reports of wolf puppies injuring each other while playing. But feel free to prove me wrong.

A litter of puppies start hurting each other (and me) as soon as they develop trazor-sharp teeth and nails, and do it over and over again. A good mom will only take so much before she distracts them, but as they get older, it gets worse, and God help them if they don't get split up before it really gets rough! (I used to breed Border Collies, the best dogs in the world but not the most aggressive by far.) Some babies kill each other (one bird will push it's nest mate out of the nest to secure all its food.) What's worse than murder? Rose colored glasses you have on, I think.

Come to think of it, they try to hurt their parents, too, but the parents put them in their place damn quickly; those are the loudest squeals. It's not all-violence-all-the-time, but there are whimpers galore. If they could use words, I'm sure they would sound just like kids. As to letting go right away, I have a puppy now that grabs onto my other dog by the tail and won't let go unless she scares him (which sometimes results in a scar). I used to have a farm; we had to dehorn the baby goats so that they couldn't impale each other later. And yes, I am an earthling.

@anongoodnurse Pushing a sibling out of the nest is not playing. If you have breed dogs, you should be aware that they never hurt each other when tumbling around. Their fur protects them from their puppy-teeth. Please, this question is about playing, not about fighting for survival.

@d-b - "If you have breed dogs, you should be aware..." I have bred dogs, do you doubt it? I don't know where you got your information from. I've observed and cared for litter after litter - six to be exact. I speak from experience.

@anongoodnurse And what is your experience? Have you ever needed to visit a vet after the puppies have played?

@d-b - It's been a month since you were downvoted (5 times). Why are you being so persistent now? You're not interested in what I think. I'm done here.

That's not answering my question. I have "worked" with two litters of puppies (terriers and spitz) and none of them come close to need a visit to the vet after playing (of course, other accidents happened: they ate things they shouldn't or stepped on broken glass and so on).

This is not a complete answer, but I couldn't fit all of that in a comment. I also don't have any expertise in neither biology nor anthropology, so you should probably take this answer with a grain of salt.
As many others here, I'm not sure that adolescent animals are really less violent than children. I used to keep rabbits and although young bunnies tend to be less aggressive, sometimes there are exceptions. If not stopped, they can mutilate each other pretty horribly.
Still, there are lot of differences between humans and other animals that affect both human behavior and your perception of it.
Prolonged childhood
Compared to other animals, human growth to adulthood is very slow. Most other mammals progress from the short period of infant dependency (toddlerdhood) directly to juvenescence. (1). Humans have 10 years of childhood.  Children are not yet fully developed, but they are already fully operational: can walk, fight and use tools. This stage is long and unusual. Other animals usually don't have a lot of time to play and be violent to each other.
Free time
Children have a lot of time to play and to fight with each other. Wild animals don't have this luxury, they have to hide from predators and provide for themselves. Less time in general means less time for play and fighting.
Pain tolerance
Children are not trained to withstand pain and tend to cry often and they do it loudly. Crying with tears coming out of the eyes is unique to humans and children cry in response to minor physical and emotional discomfort (minor falls, verbal insults). Crying child is likely to get noticed by everybody in its vicinity.
Wild animals have their own reasons to not get noticed and have to keep quite all the time, even after severe injuries. Even domestic animals have a higher sensitivity threshold and are less likely to vocalize in response to pain. Violent games between animals are less likely to be perceived as such because animals tend not to react "negatively" to them. Kittens playfully scratch and bite each other. Calves head butt one another with no mercy during play.
Society
Bear cub is expected to play with at most a couple of siblings during childhood. Young wolf grows in a pack of 5-15 other wolves, most of them adults. Herd animals live in bigger groups, but they are mostly herbivores and less likely to hurt each other during play.
Children, on the other hand, are routinely locked in small areas with hundreds and thousands other children with little to no adult supervision. That gives a lot of opportunities to pick up a fight.
To make it worse, children have human intelligence and their social interactions are extremely complex compared to juvenile animals. This provides a lot of reasons to fight and to hate each other. Lion cubs can't speak and, thus, can't insult each others intelligence and physical shape. Young dolphins are unlikely to mock each others heritage, social background, religious beliefs, political affiliation or sexual preferences. Wombat joey probably won't steal other joey's bike, etc.
The previous paragraph applies equally well to adult humans. Human interactions are uniquely complex. Animals, young and grown, can be violent to each other, but our concepts of hatred and cruelty can't be easily applied to other animals.

I suppose you're right for the best part of it, however it comes to question the generality of your statement. Dogs do become violent while playing, as are other animals. Humans are animals too, what sets them aside are community ethics. Toddlers, on the other hand, are a raw product if I do say so myself, and are animals not yet accustomed to the norms of social law. Indeed, we are a learning species, we evolve as we grow.

Dogs (and other animals) are physical when they play but that doesn't equal violent. When I was a kid, as part of a game, I threw a stone at a friend. It hit him in head and he got a concussion. I aimed for the head so it was no accident that it hit him there. I have never heard of that type of accident among playing animals.

@ d-b - Thank God dogs don't have opposable thumbs, or they'd be hitting each other with sticks as young pups.I don't know what you have been protected from, but your experience is not a universal truth.

@anongoodnurse What do you mean "protected from"? Dogs have sharp teeth and they (most of them) don´t hesitate to use them. Most animals have some kind of pretty good weapons, teeth, horns, claws you name it.


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Can you identify this species name?

I found this animal in Thanjavur.. It is millipede.. But I don't find out this species name..

Consider this: Orthomorpha coarcata
That's the closest I got, yes this millipede is found here in Odisha too
! Black and yellow millipede


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Help with identifying creature found in brazilian beach

I don't know if this is the correct place, but I've been looking for someone
that could help me identify this creature I found while I was looking for shells. There are three mollusk-like "beings" stuck in some sort of big seed (it's definitely not a rock nor a part of their body). They
 can "spin" around with the arm that is stuck in the seed, and they continuously take some blood red hair-like tentacles in and out of a shell.
I shot a video of it,  the link is right below. Please ignore all background audio, I couldn't find somewhere without people.
This "being" was found today, at roughly 6pm, washed ashore in the beach I'm visiting - "Praia Grande" in Brazil.
Another peculiar thing is that tap water makes the "things" close for a while, and sea water doesn't do much. Also, as they dried, the single tentacle hair became multiple smaller ones. They keep coming in and out, without stop.
If anyone could give me a shine on what that animal is, it would be super helpful!
https://drive.google.com/file/d/1-rSk-WVb6pkS98Npp1VF3Aq8xxXPKiuc/view?usp=drivesdk

Welcome to Biology SE. I suspect you're not getting a response to your question because the thing that makes the question answerable - the video - is at an external site. That can cause problems down the line (for instance, if Google changes its linking structures, the question becomes uncheckable). It is possible to add video to questions, but according to this question (https://meta.stackexchange.com/questions/248249/is-it-possible-to-embed-videos-in-questions), only via youtube link. Alternatively, you could take a couple of screen-captures from the video and add them.

Those are gooseneck barnacles possibly pelagic gooseneck barnacles (Lepas_anatifera).
For comparison:

A beautiful picture and description can be seen here.


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What’s the function of introns
As far as i know, introns do not encode protein products, but living creatures still have them. So what’s their function ?
P/s: Sorry for my grammar

Welcome to SE Biology. As you will see, this question has been asked before. You can find out whether your question has already been covered by searching for a term of interest like "intron". If you are on a desktop or laptop you will any case see a list of related questions in the right-hand sidebar. Also see How to ask good questions in the Help.

Eukaryotic  organisms possess introns for few purposes. One of them which i know is protein isoform formation, where different combinations of exons can give rise to different forms of the same protein  which wouldn't have been  possible otherwise , if  we only had exons. Also introns code for SiRNAs  and few other RNAs.

Welcome to Biology.SE! Your answers will be much more likely to receive a favorable response if you include supporting references (primary literature is best). In addition, please don't answer questions that have been marked as duplicates — if you have new material to contribute please post that as an answer to the older question. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively. Thanks!


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Lungs permeability
My question is:
$O_2$ and $CO_2$ pass to (in & out) the bloodstream due to difference in partial pressure and its permeability to those gases (I suppose that's why no $N_2$ passes). So, to what other molecules do lungs are permeable and what molecules can and can't pass to the bloodstream from the lungs?
Thank you.

VTC as too broad. All manner of things pass into the blood through the lungs. Anesthetic gasses like halotane, aerosolized drugs (vaping TC), CO, and too many others to list.

Nitrogen do indeed pass to the bloodstream from the lungs. That is what divers experience when breathing compressed air. It causes decompression sickness and nitrogen narcosis.

For the N2, we do not absorbe a lot of that, do we? I mean, where can I find the proportions of absorption (most of air is N2 but we don't absorb that proportion of N2 from air although N2 partial pressure is higher than O2). Do we absorbe all gases that go through lungs? Must say I'm really noob in these themes, so thank you for your answers.

When the blood is in equilibrium with the ambient atmosphere, the net transport of N2 to and from the blood is equal to zero. However, this dosen´t mean that no nitrogen crosses the blood-lung membrane, only that the amount entering equals  the amount leaving.

SOME ANSWERS HERE https://www.google.com/search?sxsrf=ACYBGNSAggw7-B8xkNYtd6-y2i70YFwopQ%3A1571218905884&ei=2eWmXa6_NZLRxgPz2oWYDw&q=MOLECULES+THAT+CAN+BE+ABSORBED+BY+LUNGS&oq=MOLECULES+THAT+CAN+BE+ABSORBED+BY+LUNGS&gs_l=psy-ab.3..33i22i29i30l2.11408.16251..16381...0.4..0.116.3507.32j7......0....1..gws-wiz.......0i71j35i39j0i273j0j0i67j0i10i67j0i20i263j0i22i30j0i13i30.GEIFqmfe_Vk&ved=0ahUKEwjuj__FvqDlAhWSqHEKHXNtAfMQ4dUDCAs&uact=5

Thank you all for the answers, it's now clearer to me.


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Meaning of a negative value for non-fiber, non-sugar carbohydrate based on a nutrition label
One of the questions for my lab is to find the non-fiber, non-sugar carbohydrate per serving of an onion. Now the total carbohydrate for this onion is 11 g, the total sugars for the onion is 9 g, and the total fiber is 3 g.
11-9-3 = -1 g of non-fiber, non-sugar carbs for this onion and this is not making any sense to me.

Welcome to Biology.SE! That could be due to rounding (e.g. more precise values might have been: 11.4 g total, 2.5 g fiber, 8.5 g sugars).  Are you restricted to using those specific labels or can you find a better source of nutritional information? —— Also, please note that homework questions should be tagged — I encourage you to take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

i am restricted to these nutritional labels sir

I got an answer faster on bodybuilding.com than i did here. WOW

Nutritional facts are rounded to the nearest unit use for measuring it, It is also only an estimation so combine errors in measurement and rounding error and it fairly easy to be off by that much.But honestly you should be asking this on the culinary stack.

@user55078 - That's not at all a surprise. Bodybuilders are rather heavily focused on many aspects of nutrition.

The values on the nutrition label from the question (11 g total carbs, 9 g sugars, 3 g fiber) could be actually explained by rounding:

Total carbohydrates: 11.45 (rounded to 11)

Sugars: 8.55 g (rounded to 9 g)
Fiber: 2.55 g (rounded to 3 g)

...which would mean there are additional 0.35 grams of non-sugar, non-fiber carbohydrates...
...BUT...
...using such a label with only rounded values (and students not knowing the exact values), does not make it possible for students to calculate the amount of non-sugar, non-fiber carbohydrates.
So, another explanation is that there is an error in either total carbohydrates (11 g - too low) or in sugars (9 g - too high; more likely 6 g), according to NutritionData for 150 grams of raw onion:

Total carbohydrates: 14 g

Sugars: 6.4 g
Fiber: 2.6 g

In either case, it seems they have used a nutrition label that is inappropriate to ask a question about the amount of non-sugar, non-fiber carbohydrates in raw onion.

The individual values in the OP's onion label are not out of line with the U.S. Department of Agriculture's reference data.  There are two of the latter, one for "Onions, raw" and one for "Onions, sweet, raw".  Their figures would lead to expecting carbohydrates of 13.8g or 11.2g, respectively, for a 148g sample.
The negative difference can be explained by simple rounding error. If the measured carbs, fiber, and sugar values were actually 11.49, 2.51, and 8.51 g then the label values would be rounded to those shown on the label, yet the difference of the measured values would be a positive value: 0.47 g.


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Does ingestion of alcohol with methylphenidate make it act more like dexmethylphenidate?
Methylphenidate (MPH) is a dopamine and norepinephrine reuptake inhibitor. It is the racemic mixture of d-MPH and l-MPH. According to the binding profile info on Wikipedia, based on studies, it is at least 6 times more potent at inhibiting the dopamine transporter (DAT) than the norepinephrine transporter (NET).
The dextrorotatory enantiomer, d-MPH, is said to be the main responsible for the therapeutic response of methylphenidate, and to be "much more bioavailable than levomethylphenidate when administered orally" (this paper from 1999 is given as reference). I read it "can be anticipated to be twice the strenght of the racemic product". One distinct property of d-MPH is that it is much less selective for DAT inhibition as opposed to dl-MPH - in fact, it is a bit more potent at inhibiting the NET (at a ratio of about 1.2 - 1.3) compared to the DAT).
The way I see it, this may have clinical significance since dopamine reuptake in the prefrontal cortex is mainly carried by the NET, since DAT expression is significantly lower in this region of the brain [1] [2].
The Wikipedia article also states that "Coingestion of alcohol (ethanol) also increases the blood plasma levels of d-methylphenidate by up to 40%". It references this study from 2011.
What I want to know is: Does that all mean that the ingestion of alcohol, when taking (racemic) methylphenidate can actually make it more potent, at least at lower doses?
Of course, alcohol has an increased activity effect on GABA receptors, which complicates things.
Thanks

Does the ingestion of alcohol, when taking (racemic) methylphenidate can actually make it more potent?
It is the 2011 study you've mentioned that answers most of the question.
In the study, ethanol co-ingestion with racemic MPH elevated maximal plasma levels of d-MPH by up to 40%. The participants reported greater stimulant effect after alcohol + MPH than after MPH alone (Table 2).
Now, the completely different question is if such combination of alco + MPH is also beneficial and safe.
Also:

MPH–ethanol coabuse has been widely reported in both annual Drug Abuse
  Warning Network data and the clinical literature.


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Can enzymes be modeled using classical mechanics?
When enzymes interact with substrates (i.e. a small ADP molecule and the much larger ATP synthase), does quantum mechanics play a significant role? Or can the interactions be relatively accurately be understood using simply classical mechanics principles?
For example, considering a free body diagram when I insert a key into a lock, the interactions between the key and the lock can be accurately modeled using simply classical mechanics (such as friction, normal forces, etc).
However, since the scale of proteins and molecules are much smaller, could the binding of ADP to ATP synthase still be accurately modeled using classical mechanics (i.e. electrostatic forces, physical contact forces, etc.)? Or are quantum principles very significant?

Related.

I think, this paper can help you understand current state of Quantum Biology and related issues.

This question may get more attention on the new Materials Modeling SE


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Spatial sequence of autumn leave colouring: top to bottom
Leave colours on trees seem to vary on the same tree from top to bottom. Leaves higher up are already further ahead in the shedding process. What's the reason for this tempero-spatial gradient?


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Folded stem on apples - does it have a name?
I have some Newton Wonder apple trees. One feature of the apples it bears is that the flesh around the stalk is occasionally elongated out of the calyx. Below is a picture that shows this on the near side.

Is there a specific name for this feature in apples?


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Is there an adhesive that could used for larval fish?
I am currently working on an experimental design that requires a larval fish (~ 4mm long) to be affixed on a metal wire tip on its dorsal side. Now, I was thinking of a glue or adhesive to do the job, but it doesn't have to be strictly these, anything that sufficiently attaches the fish to the metal wire tip would do. The glue/adhesive would have to work well on wet surface and, ideally, something that is not toxic. Any advice or ideas are welcome.

You could try methyl cellulose, which my lab and others use. It's not exactly an adhesive, but it is quite viscous. It's common enough that it's in the Zebrafish Book: https://wiki.zfin.org/display/prot/Methyl+Cellulose+Mounting . Obviously, be sure whatever you do is approved by your animal care and use committee.


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What is the relationship between r/K strategy and filial infanticides?
In other words, is the frequency of killing one's own offspring among species dependent on their location on the r/K strategy spectrum?

infanticide does not mean killing your own offspring, but offspring of your own species, the vast majority of the time animals are killing someone elses offspring. often it is a way of freeing up a mate to have your offspring.

@John You're right. That's what filial infanticide means. Google before critique.

I'm not sure if the short form is doing any favours. From your question, it sounds like you are asking "are species that kill members of their own species more likely to have 'cheap' or 'expensive' offspring?" That's still not very clear. Are you asking if infanticides in populations have been modelled before? Are you asking how to model infanticides in a population? Are you asking if the r/K spectrum is a sensible way of thinking about infanticide?

From what I can tell there isn’t any work done on this specific form of infanticide. Here is a review on the subject Here
My assessment would lead me to believe the more r selected a species is the more likely infanticide (if it happens at all) done by the individual would be toward kin. This would probably be due to a need for resources.
One thing to recall though is that this actually violates a basic inference from natural selection. Fitness is measured by how much of your alleles you contribute to the next generation. If you are eating your own offspring you are effectively reducing your fitness. The individual may however increase their long term fitness by doing this.
A possible way to locate a species that might do this would be one that sexually matures later in life but has a relatively long reproductive life with the higher number of offspring being produced in the later age groups. Finding some life history on some K selected species might help you find what you are looking for.
I’m sorry that I can’t better answer your question. and for the spelling and grammar.
cheers,

I think there is.
We know that each and every organism has sufficient resources provided by Nature for its survival.
Lets do a case study.
Let us say a population of 10 foxes lives in a jungle (whose biodiversity is undisturbed by any Non-Natural factors ).So, this particular jungle is well equipped to ensure the survival of 10 foxes.
Now, if we by any means alter the r-value - what we are actually doing is disturbing the initially stable number of organisms present in the jungle at different tropic levels.
That can occur by altering any little characteristic because all are interdependent by food webs and chains.
For eg, if the number of plants drops due to say fertility problems of the soil, then the number of herbivores would also drop (As herbivores' only source of food are plants).
This would result in competition between the carnivores for food as carnivores feed upon herbivores, whose population are dropping due to lack of sufficient food.

Competition is a type of relationship from which no one benefits.Its kinda like war- There shall be a winner but there shall be no side that doesn't suffer losses.

So, back to the situation, competition among carnivores here let's say the foxes would increase day by day as the number of plants drops. So, foxes would resort to killing their own species so as to decrease the number of organisms vying for the same food i.e here herbivores.
You know what prevails the most in nature is - The Survival of the fittest.
So, who do you think would be killed first ?
The one who has had experiences in fighting for food and such stuff or the one who is an infant i.e has not yet experienced the dynamics of the intraspecific competition

Its also worth mentioning here that of all the types of competition, Intraspecific competition is the most brutal as here organism compete for the same resources.

So, I think lesser the r-value of a location, more shall be the chances of filial infanticide.
PS: Note that I used the word chance because we can't predict 90 % of the natural things with certainty.We can make our best guesses. Say here, we don't take into account the protective nature of animals towards their offsprings.So animals are fiercely protective towards their own offsprings that they shall sacrifice themselves first while some eat their own offsprings first.

The cheetah mom is a hard-working single mother, who raises two and eight cubs at a time. In addition to feeding and teaching them, she protects them from lions, hyenas, and other predators. To keep her litter safe, the mother cheetah moves her cubs to a new location every few days.
Insects, fish, amphibians, reptiles, and birds also have been implicated in killing, and sometimes devouring, the young of their own kind.
The best example that I think I could give to you is Cannibalism. We say that Humans are the most self-conscious beings.So, if they can resort to killing their own species
  for a) food b) money (female infanticide) , then why can't animals who have supposedly lesser consciousness of their actions than humans

Thanks, I too, would incline towards K-strategists as more prone to filial infanticide but I'd say interspecific selection is stronger in r-strategists as with the greater number of individuals, there's a greater potential gain in winning this race over (as r-strategists have a greater chance of dying, fixation in the population is infinitely more valuable). My thinking is, K-strategists invest much more so it is better to end an unsuccessful trial than to continue it for the rest of your life. But I can't evaluate all the other effects.


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What kind of object is this?
I'm unsure whether to call it a fruit or a vegetable. I found it on the road in a neighborhood and decided to pick it up before a car squashed it. (Thus, my initial guess was a squash.)

Should be a Papaya, thus a fruit, an outline of your geographical location would be helpful to determine it.