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Is it possible to rank standardized beta coefficients in general linear mixed model?
I have an experimental treatment at 15 sites and would like to build models to associate usage rates of 4 species with a set of 6 explanatory variables. In the end, I would like to rank the importance of these variable for each species.
Ordinarily, I would simply fit the models and then standardize the beta coefficient by dividing by the standard error and ordering by absolute value.
However, in this case, I need to model a random effect of site and my response variable must be modeled as zero-inflated Poisson, which takes me outside of the realm in which I've seen this comparative analysis performed.
Is there an analogous procedure to ranking standardized beta coefficients for generalized linear mixed models?
Much thanks in advance!
Is it possible to rank standardized beta coefficients in generalized linear mixed models?

I think this is probably a better fit for stats.SE. The nature of the variables won't matter to them there, only the structure of the data and models.

@kmm , that is a good point. I thought I would ask here first since this is a fairly common issue in ecological modelling (as judging from the conversations I've had with folks in my university cohort) that I suspect either someone has already dealt with, or others in the biological community, would benefit from.

I'm voting to close this question as off-topic because it belongs to stat.SE.

If I understand you correctly, you should be able to standardize the explanatory variables (zero mean, unit sd) before the analysis (at least if the explanatory variables are continuous). Then the effect sizes can be compared between predictors that have different scales.

Also, the "importance" of variables is a bit ambiguous. A variable can have a large effect size (top-ranked coefficient), but without a fair amount of variation in that variable it might not have a large effect in practice. On the other hand, a variable with a smaller effect size but a larger variation between sites can explain more of the variance in the response.


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What is the number of species known through paleontological evidence?
Essentially, this question could also be asked: how many species do all of the paleontological specimens in collections (or collections records) represent?
I recognize that species is a temporal concept when thinking about differentiation across time; but, natural history collection catalog specimens to species level, so there must be a reasonable basis to make this distinction.
Also, note that I'm not exactly interested in inferred species (i.e. if we have records of species A and species B, we might infer a last common ancestor, species C).

Very interesting question.
I remember reading about it in one of Stephen Jay Gould's great books (The Panda's Thumb? The Flamingo's Smile? Wonderful Life: The Burgess Shale and the Nature of History? Dinosaur in a Haystack? Probably in one of these).
He wrote exactly about this question, and the effort made by teams from many different countries to get to an "approximate" result. What really impressed me at the time (fifteen years ago) is that when Chinese scientists were invited to add material for a second analysis, the number of known fossil species doubled!
Please, if anyone find the exact source of this, I'll be glad to read it!
But maybe you can get an idea by looking at the number of fossil species for certain groups, and comparing with the number of estimated/known extant species. Keep in mind the rates of fossilization for each group, and also the fact that Nematoda and Acari might be the most overlooked groups in terms of species number (both seem to parasitize animals through most of the Animal Kingdom).

Short answer no one knows exactly, a single database of fossils does not exist. there are lots of specialized ones, for say pollen or dinosaurs, but not one complte one. each museum maintains their own. There are estimates based on type specimen publications but they tend to overemphasize some groups like vertebrates and under represent less... charismatic groups.  Accroding to this study http://www.pnas.org/content/99/6/3706.full
There are at least 280,000 named invertibrate species, (infered species are not given species names) hopefully that gets you started. This is a recognized problem and there is a lot of debate about how to fix it.

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Current scientific theories for evolution of Cucurbita
I'm attempting to find research on scientific theories surrounding the evolution of certain plants, and am unable to find any footing with respect to a certain genus.
In this case, I am researching Cucurbita (ie: squash, pumpkins, etc), and can't find any basis for how it survives inherently without outside manual intervention. Unlike hot peppers (eg: Capsicum annuum), it is not easily ingested by birds, who do not suffer from the painful effects of capsaicin, and effectively transport the seeds, undigested, to new areas to spread the plant.
Also, unlike fruit growing on a tree, such as apples, it doesn't (seem) to provide a means to transport seeds any meaningful distance.
Finally, it seems most animals; ruminants, scavengers, and insects alike, would consume and digest the seeds.
Are there any generally-accepted (or at this point, plausible) theories with research to back it with respect to how such plants could survive long term without being manually grown and harvested by a species which eats them? While I understand (and acknowledge) the scientific theory of evolution, I'm not sure how the survival of such plants seems to be a special case.
Thanks!

I don't remember much, had studied botany a long time ago. But isn't cucurbitaceae that genus where the fruit blasts to disperse the seeds?? Then you dont need animals to eat taht stuff..

Many plants that we use for have gone through thousands of generations of intensive artificial selection

Sorry, should be family cucurbitaceae

@DavidBlomstrom Very interesting read. It does coincide with this question, but it seems the information on the mechanics and history of the subject elude me.

@DavidBlomstrom I just found some articles by adding "extinction" to my searches that indicate the same case with avocados (lack of mega mammals to transport the seeds via their dung). My mistake was assuming the seeds would be destroyed via digestion. It seems humans did indeed help it survive after large mammals started to die out, like the avocado. If you'd care to re-create your comment as an answer, I will mark it as accepted. Cheers!

@rg255 I'll agree 100% with you on that. Please don't mistake me for a theist trying to find a smoking gun or counter-example to evolution (ie: "checkmate atheists!"). I'm genuinely interested in how these species survived.

I would maybe change the title to something like "Seed dispersal in Cucurbitaceae"

Don't worry @Dogbert I was only giving a hint as to why it may be hard to see an adaptive point to many features of crop plants (and domestic animals for that matter; dogs and cats are very different from wolves and lions!)

You're right that modern species would have a hard time spreading group seeds, though you're not quite right about the reasons.  Cucurbita rinds are extremely bitter, so that modern mammals are reluctant to (or unable to) process the rinds to access the seeds.
According to a recent article (Gourds and squashes (Cucurbita spp.) adapted to megafaunal extinction and ecological anachronism through domestication), the explanation is that wild Cucurbita first co-evolved with North American megafauna, like mammoths and mastodons, who could tolerate the toxic/bitter rind. (The authors also suggest that megafauna also produced suitable habitats for their growth.)
Following the extinction of these megafauna, humans picked up the slack, with most wild Cucurbita going extinct and only domesticated versions remaining.

Collectively, these results point to wild-type declines coinciding with widespread domestication. ...megafauna consumed Cucurbita fruits and dispersed their seeds; wild Cucurbita were likely left without mutualistic dispersal partners in the Holocene because they are unpalatable to smaller surviving mammals with more bitter taste receptor genes. ... Thus, anthropogenic landscapes provided favorable growth habitats and willing dispersal partners in the wake of ecological upheaval.

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if sperm contains only 50% of someone's DNA how can it be used to identify someone?
Is DNA so unique that 50% of it is enough to identify a single person?

any single sperm cell contains half the DNA, but a typical sperm sample has many millions of cells, so in total, the entire DNA is available.

You make one mistake: The set of chromosomes in sperm and egg cells is haploid, this means that there is only one copy available in each cell instead of two.

@user137 Every sperm cell has the complete set of genes. But only one copy instead of two. So each sperm cell is enough to identify its owner.

@Chris It's way late here, I'm tired. And how often does someone ID a person based on a single cell?

@user137 For forensics this happens.

@Chris In a forensics example, are they finding a single cell, isolating its DNA, then running PCR, or do they just run PCR on a sample and hope that at least a single cell's worth of the suspect's DNA is in there?

@user137 I know a case from Germany where terrorists left one or two hairs at the crime scene. These were sucessfully used to identify the person who lost them. I am not too much into crime forensics, but here you have to amplify the DNA first. And make sure you have no contaminations.

Your both wrong- there is no guaranteed 100 percent proof to ID someone from DNA. look into the numbers generated to give the 99 percent chance. They say million to 1 in that persons ethnicity group.There is no way to identify a humans ethnicity either.

@TheVoid There are issues with DNA identification, especially if the lab is doing a sloppy job, but DNA has to be more reliable and objective than fingerprint identification or eyewitness reports.

The comment from @User137 pretty much gets it: the mix of all sperm cells in even a small sample will contain the whole genome on average. So in the hair example in the comments above, there are probably a good number of dead cells hanging onto the hair, enough for analysis. Meiosis will redistribute the DNA sequences inherited from mom and dad randomly, so each sperm is in theory a unique patchwork of that person's genome, but overall the genome will be covered well. Single-cell work, on the other hand, is technically very challenging.
[edit: here is an article describing methods for low-input analysis of forensic samples. Unfortunately paywalled.]
To directly answer the OP on uniqueness: absolutely a single sperm is that unique for each person, in principle. There are lots and lots of genetic variants in each human, and everyone represents a unique mix. It is estimated that 1/1000 places in the genome of each person differ from any other person, on average (for substitutions). there are 3*10^9 places in the genome for this to be the case, which gives you a very large number of differences, ASSUMING that you can actually ascertain all those differences. [edit: for a discussion of these stats see here.]
The technical problem with forensics is that often they only look at a few places in the genome (microsatellites usually), because it is relatively expensive and hard even with recent technology to look at more than that in any detail. This leads to the non-trivial possibility of misidentification with the standard battery of loci. This possibility never goes away entirely, but it becomes very small with more data. I am not a forensic scientist, possibly they have gotten more comprehensive or the methods have changed in recent times.
[edit: here is a document that has what appears to be a readable introduction to DNA forensics, including technical discussions of some drawbacks of marker panels used by for instance the FBI of the USA.]

It would be more difficult to identify someone from a single sperm cell, rather than other cells contained in their semen.
However, if we are just comparing the DNA from any diploid cell in the body, you run electrophoresis to compare DNA samples.
For example, if you wanted to establish the paternity of a child. You would collect a sample of the child's DNA, the mother's DNA and the possible fathers' DNA (usually all from cheek or hair cells).
PCR would be carried out to replicate each sample into a large quantity.
You would then use the same restriction enzyme in each sample to cut the DNA in specific places along the sample.
Each sample is placed in an individual well at one end of agarose gel, immersed in a buffer solution, and a current passed through (cathode at the well-end, anode at the opposite end).
As DNA is negatively charged due to phosphate groups, it travels towards the anode, through the gel. Shorter fragments of DNA travel faster in the set time the electrophoresis is run for.
Southern blotting is then used to establish a banding pattern of the fragments of DNA - you rule out the bands that the child and the mother share. To establish paternity, you identify bands that the child shares with each possible father. The father whom the child shares the most bands is the most likely father.

Welcome to Bio. Isn't DNA profiling done with PCR and detection of SNPs? I'm not an expert here, but your answer reads like an undergrad biochemistry assays handbook. The question is not so much how it's done, but if it can be done given the properties of the DNA in gametes and diploid cells.


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What are extracellular matrix pathways?
I was reading a research paper dealing with acute myeloid leukemia and the term "extracellular matrix pathway" came up. What does it mean? I found literature on extracellular matrix, but I'm not sure what the "pathway" indicates.

Can you add a link to the paper? This might help.

@Goldname read this one, http://joe.endocrinology-journals.org/content/209/2/139.full

Sorry, I can't link it because the paper is not available online yet

Can you at least [edit] your question and add a paragraph or two of context?


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Do antagonist-receptor complexes get absorbed into the cell?
My understanding is that normally, a neurotransmitter binds to a receptor and then that ligand-receptor complex gets absorbed into the cell and either degraded or recycled. So does the same thing happen when the ligand is not the endogenous neurotransmitter, but instead an "artificial" antagonist -- like, say, bupropion bound to a nicotinic receptor?

When a neurotransmitter, like serotonin, binds to it's specific receptor, the ligand-receptor complex is not phagocytosed.  Picture the human cell membrane and think of the serotonin receptor like a long piece of rope that has been wound up, but is embedded inside the cell membrane forever.  After the serotonin binds, the structure of the receptor changes, causing lots of steps to start (like a domino effect) where molecules are released from the inner aspect of the receptor, thus carrying the message into the nucleus.

Are you saying that 5-HT receptors don't internalize? This answer may need a little more research.

What kind of molecules internalize? Are we talking ions?


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How does receptor downregulation/upregulation work?
My understanding is that if a cell is flooded with a certain neurotransmitter, it may decrease the density of that neurotransmitter. What I don't understand is how.
Is it a direct physical result of the receptor-ligand complex being internalized? I.e., the receptors simply aren't there anymore, because they've been internalized?
Or, does the internalization of specific receptor-ligand complexes actually get sensed by the cell somehow, causing it to produce fewer receptors in the future?

Both internalization (sometimes with degradation) and changes in gene expression can occur; the circumstances leading to the down regulation determine which (or both). It isn't necessary for receptors to be bound to their ligand to be internalized, though, and it isn't the internalization of receptors that causes changes in gene expression (I suppose it is possible that happens someplace, but not that I am familiar with). The processes involve activation of second messenger systems and kinases that either phosphorylate/dephosphorylate the receptors to mark them for internalization and/or degradation, or activate/deactivate transcription factors.
Here are two reviews with more information: one is newer but focused on a single class of receptors and fairly in-depth; the other is a bit dated but more broad, but brief:
Williams, J. T., Ingram, S. L., Henderson, G., Chavkin, C., von Zastrow, M., Schulz, S., ... & Christie, M. J. (2013). Regulation of µ-opioid receptors: Desensitization, phosphorylation, internalization, and tolerance. Pharmacological reviews, 65(1), 223-254.
Tsao, P., & von Zastrow, M. (2000). Downregulation of G protein-coupled receptors. Current opinion in neurobiology, 10(3), 365-369.
You can also read about long term depression, which is different from homeostatic responses to ligand concentrations, but it does seem to serve a homeostatic function to keep overall synaptic strengths from growing indefinitely, and the molecular pathways are very similar (and it is a very well-studied phenomenon so you will find a lot of accessible information).

> internalization of receptors that causes changes in gene expression
EGFR translocation to the nucleus was an example that came to mind (ref).

@CMosychuk Thanks for the comment, it's a good opportunity for a clarificaiton. Yes of course, there are receptors for which internalization itself (after binding a ligand) is a signalling mechanism. I was referring only to the homeostatic regulation of membrane receptor concentrations in response to excess ligand, as in the OP. I wouldn't consider receptor internalization as part of a regular signalling pathway to be part of that homeostatic regulation. But thank you for pointing out that internalization can be a signal, I didn't mean to imply that it isn't elsewhere.


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Where in the nervous system are synapses chemical, and where are they electrical?
Paraphrased from the Wikipedia article "Synapse":
There are two fundamentally different kinds of synapses:

Chemical synapses, which convert electrical activity in the presynaptic neuron into the release of neurotransmitters via the activation of voltage-gated calcium channels. The released neurotransmitters, which vary in type by cell, bind to receptors of the postsynaptic cell, giving rise to complex behaviors.
Electrical synapses, in which presynaptic and postsynaptic are connected by "gap junctions" or synaptic clefts capable of passing electrical current, resulting in rapid signal transduction.

Are there certain structures and locations in the nervous system that are mostly or exclusively chemical synapses, and certain ones that are mostly or exclusively electrical? Or, are they mixed throughout the nervous system?
For example, one might suppose that the neurons which transmit signals from brain to limbs might be electrical, due to the apparent advantage of fast transduction times in this scenario. On the other hand, it might be advantageous for the brain to be capable of more the dynamic, albeit slower, signal transmissions made possible by chemical synapses. Are these intuitions accurate?

Synapses are almost all chemical, the electrical synapses are more of a "special case".
The speed of transmission across limbs, etc, has very little to do with the speed of the actual synapse. The signal itself is conducted electrically inside a given cell (this is an "action potential"), aided in many cases by insulating myelination. The synapse is just the endpoint.
Some places where electrical synapses/gap junctions are present are:

Between cardiomyocytes, to synchronize heart contraction
Between certain networks of inhibitory interneurons in the CNS
In some (but not nearly all) reflex circuits


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Is this a simple Hardy-Weinberg problem?
Phenylketonuria is a severe developmental disability due to a rare autosomal recessive allele. Approximately 1 in every 10,000 newborns suffer from this disease. Calculate the frequency of the allele causing this disease and the frequency of heterozygous "carrier" individuals.
What I've come up with is that this is a Hardy-Weinberg problem. Is this true?
My answers:
frequency of allele causing disease = 0.01
frequency of heterozygous "carrier" individuals = 0.0198

Yeah you are right but what are your reasons for thinking that this is a Hardy weinberg problem ?

I honestly have no idea. I just tried the numbers that semi made sense and it seemed to answer the questions at hand. Is there a method that reveals why this is exactly a Hardy-Weinberg problem?

See my ans. And yeah I also think this is the "bestest" site ever !!

Yes, your answers are correct. Of course, your calculations forced you to make the standard Hardy-Weinberg assumptions such as random mating. Good job!

This should be a comment.

Well... The OP is asking did I get it right? The answer is either no, because... or yes.

Too long for comment :
If you want to solve the question by Hardy Weinberg, there are certain assumptions involved :-
1.There is random mating. People do not choose their mates on the basis of whether they carry PKU gene or not & mating among close relatives is not there.
2.No new PKU mutations happen.
3.There is no difference in the reproductive capacity of people with or without PKU gene.
If your study population fulfills these criterias, you can apply Hardy-Weinberg to calculate frequencies of various genotypes.
Because this question is  homework ,such assumptions are not mentioned. And, at undergrad level,there is no other concept by which you can solve this question except HWE.
PS: Try to think what would happen if these assumptions are not fulfilled.
PSS: Even if you are solving a small homework question, do think about the logic behind every step. Though it may seem like a lot of work initially , it has enormous potential to teach you subtle concepts !

The fact that PKU is a "severe developmental disease" makes me think that assumption #3 is violated. It could be that the students are meant to solve the problem with the HW equation anyway, though

@cactuswoman If PKU is diagnosed early and diet restrictions are followed, it is possible to live "normally".


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Why do workouts cause your muscles to feel heavy?
I know that muscle activity causes your muscles to build up lactic acid. Is this the specific reason that your muscles begin to feel heavy? How does this relate to the healing or inflammation process for muscles, or does it?
Thanks!


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What is the structural/chemical difference leading to different shapes in facial/head/pubic hair?
Different hairs have different shapes, thicknesses, properties.
What exactly is different between these types of hairs? a previous post implies that the root of the differing length (pun intended) is the rate at which the skin sheds the hair. However, this doesn't explain the different degrees of curliness, thicknesses, and textures.

hair shape texture is really easy. the biggest effect is the shape, size, and angle of the hair follicle. Hair with different cross sections have different properties. If hair is stiffer in one plane than other it will tend to bend along the weaker plane. Larger follicles will of course produce thicker, thus stiffer hair and the angle of the follicle can influence the hairs cross sections as mush as the follicles cross sectional shape can. Note the chart below is simplified triangular and kidney shaped cross sections also exist.

This is a nice picture, where did you find it?

Out of one of my lessons, let me see if I can find the original source. here it came from this forensics slide show. https://www.slideshare.net/leahmorgan/forensics-ch-5-6-notes

At one time I donated a "pinch" of head hair some years ago. A crossection was made with a microtome. The point being that there were many more colors that the photo above; white,black,red, and a dozen shades of tan/brown. My hair was nominally light brown. ( a much better photo also).

Similar to the differences between curly and straight hair, different hairs have different hair follicles.
Sex hormones at the onset of puberty rebuild the local vellus hair into terminal hair, which tends to be longer, thicker, and darker. The anagen/telogen/catagen cycle is different for these follicles and as a result they get longer.

you really should go into what differences their are in follicles.

As far as I can tell terminal follicles are just bigger?


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Can the negative afterimage appear only if there is light or is it possible in darkness?
Reading the following paragraph:

After staring at the red and blue shamrock, you saw a green and
  yellow afterimage. Opponent-process theory proposes that as you stared
  at the red and blue shamrock, you were using the red and blue portions
  of the opponent-process cells. After a period of 60 to 90 seconds of
  continuous staring, you expended these cells' capacity to fire action
  potentials. In a sense, you temporarily "wore out" the red and blue
  portions of these cells. Then you looked at a blank sheet of white
  paper. Under normal conditions, the while light would excite all of
  the opponent-process cells. Recall that white light contains all
  colors of light. But, given the exhausted state of your
  opponent-process cells, only parts of them were capable of firing
  action potentials. In this example, the green and yellow parts of the
  cells were ready to fire. The light reflected off of the white paper
  could excite only the yellow and green parts of the cells, so you saw
  a green and yellow shamrock.
(Ellen Pastorino & Susann Doyle-Portillo, What Is Psychology? Essentials, 2010)

I've been wondering:
Can the negative afterimage appear only if there is light or is it possible in darkness?
In other words does the red color make the ganglion continue working even when there is no image and the afterimage appears green or is more light required in order for the afterimage to appear?

Glutamate release from photoreceptors is inhibited by incident photons (ref). During photobleaching, assume that the effect of an incident photon drops to zero. The implication then is that if all light is removed subsequent to selective photobleaching, there will be no difference in activation between bleached photoreceptors and unbleached photoreceptors. This observation suggests that no afterimage will be visible in darkness.
But there might be rebound effects or other effects of light adaptation that will result in a perceivable afterimage in darkness. Certainly there are hallucinatory visual patterns than can be generated cortically, suggesting that a cortical afterimage could be generated in darkness.


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What would be the impact of depositing limestone in the oceans (to reverse acidification) on ocean life forms and biodiversity?
This question asked: What is the evidence it is feasible to reverse ocean acidification by adding large quantities of a base (bicarb soda)?
The result was:

Danny Harvey of the University of Toronto has already looked into this. His solution is to deposit 4 Gt/yr of limestone into the oceans. To put this in perspective, global coal production in 2013 was nearly double this at 7.823 Gt and it is more than global iron ore production in 2014 of 3.22 Gt.

The respondent then posed the question: What impact would such a huge annual deposition of limestone have of ocean life forms and biodiversity?
My question is: What would be the impact of depositing limestone in the oceans (to reverse acidification) on ocean life forms and biodiversity?

Harvey recommended 40 µm powdered limestone, delivered to certain points and depths in the oceans. The amount of fossil fuels consumed to mine, powder, transport, and precisely deliver the limestone each year would necessitate a much larger quantity of limestone to offset it, increasing fuel use even more, requiring more limestone, and on and on, not to mention the amount of machinery, trains, trucks, and ships that would need to be produced to even put this operation into effect. This idea is completely unfeasible, so I'm voting to close this as opinion-based.

From What types of questions should I avoid asking?: avoid asking subjective questions where (…) you are asking an open-ended, hypothetical question: "What if ______ happened?"

To simplify, acidification of oceans is due to excess anthropogenic carbon dioxide CO2:

H2O + CO2 → H2CO3 → H+ + HCO3-

Seawater is naturally saturated with another base, carbonate ion (CO32-) that acts like an "antacid" to neutralize the H+, forming more bicarbonate.

CO32- + H+ → HCO3-

You want to alkalinize the ocean by dumping CaCO3. That sounds pretty good, and not only would it add more buffer (and decrease acidification) but it would also help the sea creatures which use dissolved Ca2+ and CO32- to make shells of calcium carbonate CaCO3. (The other effect of excess CO2 is the leaching of CaCO3 from shells and corals or other marine organisms:

CaCO3 + H+ → HCO3- + Ca2+

The limestone mined today is used for gravel, in concrete, road surfacing, foundation support beneath weight-bearing structures, the boulder faces of earthen dams, Portland cement (N.B. the burning of limestone in the cement-making process liberates CO2 gas), Aglime (pulverized limestone) and quicklime (process liberates CO2 gas) which are both soil stabilizers, hydrated lime used to filter potable water supplies and to treat solid and liquid waste and in processing petroleum. These are only the major uses of limestone.
The average annual limestone production in Missouri (the largest deposit of limestone in the world) is about 89 million short tons/year. The cement industry alone is a MAJOR producer of CO2. Producing a ton of cement requires 4.7 million BTU of energy (some of which will release CO2), equivalent to about 400 pounds of coal, and generates nearly a ton of CO2.
So, in addition to the CO2 produced by the use of limestone in everyday life, you want to mine it and dump it into the sea. Unfortunately, even finely ground limestone (remember all that CO2 it takes to mine and crush it) is poorly soluble in water (pH 7.0). It does increase with acid, but still is very slow. Also, it sinks. The worst acidification of the ocean is in surface waters.

Some estimates suggest that close to 100 million tons of limestone are mined globally each year. (It's probably much more than that; see Missouri alone.) You want to mine, crush (to between 40µm - 10µm!!), and deliver an additional 4 Gt/yr of limestone, even though in the paper you cite, that amount per year would not help:

Extraordinary additional measures (adding 4 Gt limestone/yr to the ocean for > 200 years) provides a modest additional benefit (additional to cutting CO2 emissions.)

Why? What difference would knowing the effect on biodiversity be when just procuring, processing and delivering the stuff would generate more CO2 than it could possibly buffer, and would have a minimal effect anyway?


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Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?
I've had friends see the boat and giant teeth of a giant shark attack of a boat in Japan. (Teeth larger than a great white). [I can't find anything about this on the Internet].
In addition, this report from Pakistan seems to suggest that there are large sharks in the deep of the Oceans.

15-TON PREHISTORIC SHARK CAPTURED OFF COAST OF PAKISTAN

Karachi | A giant prehistoric shark previously thought to be extinct for more than 20 million years has been captured by local fishermen off the coast of Pakistan, reports the Islamabad Herald this morning.
The giant creature first thought to be a great white shark was rapidly declared by experts to be an unknown species of shark as it’s great weight and size were unheard of. Analysis of the teeth suggest the shark to be a parent of the Megalodon, an extinct species of shark that lived approximately 28 to 1.5 million years ago, during the Cenozoic Era.
The sea creature that measures an incredible 10.4 meters and weighs an astounding 15.6 tons is the largest living shark ever caught to date, great white sharks reaching an impressive 7 tons at full growth, a size that is no match for this giant prehistoric shark that can reach an imposing 20 meters in length and possibly weight up to 30 tons, depending on estimates.

My question is: Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?

Not exactly an answer, but about 95% of Earth's oceans are unexplored, so I would say that it is pretty likely that there is something, or somethings, that are bigger than currently discovered sharks are alive somewhere in this world. Also, organisms like crocodiles have existed since before the dinosaurs. There's more shark friendly land than crocodile friendly land. If a croc can live 200 million years, then why couldn't a shark?

As an aside, even assuming arguendo that the shark is real, it cannot be the parent of Megalodon, only a descendant or a relative.

The "Cenozoic era" includes the present, so that isn't helpful. Also, technically, since "historic" times only go back a few thousand years, virtually every species, let alone every shark species, is "prehistoric".

No.
The article linked to is a hoax, and was debunked by Snopes.
The website is known for its hoaxes and satirical articles, and it states itself that its articles are faked.

WNDR assumes however all responsibility for the satirical nature of its articles and for the fictional nature of their content. All characters appearing in the articles in this website – even those based on real people –  are entirely fictional and any resemblance between them and any persons, living, dead, or undead is purely a miracle.

The image of the shark was taken from a 2009 photograph of a great white shark caught in South Africa. The shark was reportedly 4.3m long, a normal length for a great white shark.
The large apparent size of the shark as compared to the fisherman is due to a trick of perspective. This article shows the shark in perspective in a second image, which clearly shows that it is not as large as it apparently is in the first image.


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What is the evidence that mammals are unable to process excess sodium chloride?
I grew up hearing the mantra

excess salt causes heart disease

I had a vague understanding that it caused deposits in the body or something. Now that I give it more thought - I come up with three vaguely plausible explanations for this:

kidneys have a fixed limit on how much sodium chloride they can filter from your bloodstream in a day
excess salt has an effect on oxidation/redux reactions or acid/base levels that means your body's chemical reactions aren't performing optimally
the excess ions mess with other reactions in the body

When I take the 'devils advocate' argument in my mind - my plausible arguments are:

how can salt cause deposits in the body? It would simply dissolve in the bloodstream
surely the body has sufficient chemical mechanism to flush out surplus sodium ions

Now the author here makes the following claim:

The entire field of research around salt is a colossal [stuffup], for a fairly simple reason: sweat is salty. If you sweat, due to exercise or high temperatures, you lose about 1g/L of sodium. So right off the bat, all the research that's trying to find a population-wide correct amount of sodium to eat is on a wrong track, because there's no such thing.
But it's even worse, because most of the research doesn't measure the amount of sodium people take in through food, it measures the amount of sodium they lose in urine. This isn't their intake, it's what's left after losses, so it's confounded by exercise.
And it's even worse than that, because while the actual studies indicate that there's no benefit from cutting salt intake, some high-status organizations once said there was, and are acting as though they can't take it back without losing face.
The overall result is that there are a bunch of people shouting "less salt!" and a bunch of people shouting "the same amount of salt!" and no one has any model of how much salt they actually need, so they occasionally end up deficient.

In addition, the article here claims:

...there are the epidemiologists whose research appears to point in the other direction. They track the connection between salt and deaths from heart attacks and strokes, and their studies indicate that while heavy salt eaters did die sooner, there is little evident danger from the average American’s intake.

My question is: What is the evidence that mammals are unable to process excess sodium chloride?

Good question. I don't know the answer, but this article http://www.scientificamerican.com/article/its-time-to-end-the-war-on-salt/ claims that there is no consensus in the field that high salt intake has any adverse effects.


text:
Mother's physiological response to baby crying
I have read several articles [1,2] that talks about the physiological response in mothers when their babies cry. Is there any studies performed and published that show that this is not true ?

https://www.sciencenews.org/blog/growth-curve/how-baby-cries-bore-mom%E2%80%99s-brain
https://www.livescience.com/36964-baby-cries-women-men-brains.html

Hello Noor. It is better to cite a peer reviewed publication when citing references. Anyway, to prove that something exists you just need a single evidence; to disprove the existence of something you have to exhaust all possibilities. First, step to verify the authenticity of a research is to check if it is designed and conducted properly. Then you repeat the experiment and see if it is reproducible. Having said that, I would insist that you should also try looking for articles that dispute this claim. Here, we appreciate if users show some effort from their side before asking.

Some women do not respond emotionally and physiolocically to their own crying infants. It is highly abnormal, and deleterious to the emotional development of the child. Women are hard wired to resopnd to their infant crying. If it weren't true, we would not have survived as a species.

@WYSIWYG, i take note of your advise, thanks

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


text:
When sperm and egg mix, are the genes rearranged?
I remember once my high school teacher said when the sperm fertilizes the egg the genes are mixed very randomly, is that true?

It is rather wrong! Segregation and recombination both occur at the moment of the formation of the gametes (meiosis) and not at the moment of the fertilization. You might want to have a look at the wiki articles for meiosis, recombination and segregation.

Your question is unclear. Perhaps you should clarify with your teacher about what exactly they wanted to say. Or otherwise you should clarify what you really mean by "mixing"? Sure, because of diffusion, the paternal and maternal chromosomes would be uniformly distributed in the nuclear space.

No.  When sperm and ova are forming, the chromosomes you inherited from your mother lines up with the chromosome you inherited from your father, and "crossing over" happens.  It would be like taking a Merriam-Webster dictionary, and another brand of dictionary, and picking a random point (like say, the middles of the "C" section), cutting both books at that point, and joining the portion of one with the portion of the other, making new books that are part Merriam Webster, and part the other kind of dictionary.  That happens in every chromosome, and the gamete is made up of those franken-chromosomes.


text:
Units of parameters in epidemiological model
The simplest malaria model is given by $$\frac{dI}{dt} = \frac{\alpha \beta I}{\alpha I + r} (1-I) - \mu I$$
where $\mu$ is the death rate of humans, $\alpha$ is the transmission rate from humans to mosquitoes, $\beta$ is the transmission rate from infected mosquitoes to susceptible humans, and $r$ is the natural death rate of mosquitoes.
Assuming the units are given in $d^{-1}$, or per day, we can assume $r$ to be rather large, given that it isn't part of a larger product (and thus isn't a proportion). We can thus assume $r$ to be anywhere from a few dozen to a few hundred, depending on the size of the population. Recall that this is the amount of mosquitoes killed per day.
$\alpha$ is the transmission rate from humans to mosquitoes, and does appear to be a proportion, so $0 < \alpha < 1$. Thus, $\alpha$ is the probability a mosquito not carrying malaria bites a human $\textit{with}$ malaria. Assuming nothing more than 15% of a population of humans has malaria, and that 95% of a mosquito population do not carry malaria, this is $0.15*0.95 = \alpha = 0.143,$ or a 14% probability.
$\beta$ is also a proportion, and is the transmission rate from infected mosquitoes to susceptible humans. Rather, $\beta$ is the probability an infected mosquito will bite a human. Assuming a generous mosquito population (a few thousand at the least), we assume that about 5% carry malaria and (based on our previous assumptions) they have a 85% chance of biting a susceptible human (given that 15% are already infected). So $\beta = 0.05*0.85 = 0.0425$.
$\mu$ is given as the death rate of humans. Neglecting deaths by reasons other than malaria itself, we assume this value to be about $0.3\%$, given 627,000 deaths in 2012 out out of an estimated 207 million cases that year.
Is this analysis correct? If not, where can I find values for the above parameters? Are there any case studies where I can calculate the above values?
Thank you in advance.


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how does one apply for masters in genetics abroad?
Please can some one give me step wise instructions for applying for a masters degree in genetics or biological sciences?

This may be more on-topic in Academia SE!

I am voting to close as off-topic. The question would be on-topic in Acedemia.SE.

A bit more than a year ago I applied for a PhD position abroad in population genetics. Here are my steps: 1) Find a supervisor that a) does the kind of things I like, b) is good, c) is friendly, d) has trained people who got job in the academia. 2) Read some of his/her recent and most cited papers, 3) Evaluate the place 4) get a rough idea of what you would like to work on, 5) Contact him/her 6) If (s)he showed interest in your application, go through the formal application.

Note that it will take some time reading on the website to understand a new system. I have studied in 4 (or 5) different universities in 3 (or 4) different countries. It always take some time to get used to a new system. Your supervisor (and/or future lab mates) will be happy to help you.

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text:
Why is there an apparent reduction of reptile species near the Mississippi River?
The USGS Gap Analysis Program published a map of reptile species richness in the U.S. There is a conspicuous reduction in reptile richness along the Mississippi River corridor. Why might this be?

From USGS:

This map of reptile species richness in the U.S. is derived from the
  USGS Gap Analysis Program’s (GAP) national reptile ranges dataset. The
  map represents the total number of reptile species summarized by
  12-digit hydrological units (HUCs). Light blue HUCs have the lowest
  number of species while red HUCs have the highest.

Is it possible this reflects relatively intense human influence (farming, cities, industrialization) in the Mississippi delta?  This map suggests there are "26-43" species in the region, whereas a 1955 paper (Notes on Mississippi Amphibians and Reptiles) claimed to identify "89 species and subspecies as follows: Salamanders, 14; frogs and toads, 19; lizards, 8; snakes, 36; and turtles, 12."

Interesting information @iayork. But did you find any numbers on species richness for the surrounding areas of similar latitude? It could also be that numbers fell proportionally in all areas around the river.

The reptiles mostly were ploughed away and replaced with soy beans.

The low reptile diversity zone matches the Mississippi Alluvial Plain which includes the Mississippi Floodplain. The Mississipi drains nearly half of the USA's geographic area, so the flood plain is massive.
The Silt Plain is very flat, mostly has hills left by oxbow lakes and river meanders. If you put your hand in the ground, it consists of organic matter/silt/clay/mud/fine sand, and it is very fertile until it is depleted by modern agricultural practices.
It's one of the more productive agricultural regions in the USA, and it's mostly giant square fields and mono cultures.
zoom in: http://gokml.net/maps#ll=32.163208,-91.720681&z=11&t=h&q=winnsboro
Here is a quote from the Discussion at the end of this review:

traditional agricultural landscapes, typically characterized by
  mosaic–like structures, intermediate levels of disturbance, and able
  to host great biodiversity levels (Bignal & McCracken, 1996), have
  undergone profound transformations in last decades. The rapid
  extension of intensively cultivated fields and the reduction and
  fragmentation of the original habitats have led to the creation of
  more uniform and depleted landscapes, with significant loss of
  biodiversity (Whittaker, 1975; Bull & Skovlin, 1982; Burel et al.,
  1998; Zechmeister & Moser, 2001; Moser et al., 2002; Pfiffner & Luka,
  2003). In accordance with these changes, our analysis of reptile
  assemblages in an agricultural area mainly devoted to the intensive
  cultivation of arable lands found the landscape to be relatively poor
  in biodiversity. Four out of five agricultural land uses hosted only
  one species, while most of the recorded reptiles occurred inside a few
  patches of semi–natural habitats and, above all, in the grid of
  vegetated buffer strips interspersed among the cultivated lands. In
  addition, during field activity, we observed only seven of the
  eighteen species of terrestrial reptiles reported for the province
  where the sites are located, and most records were ascribable to a
  single species.

Reptiles and Amphibians are at the top of the insect food chain, and studies have shown that they are sensitive to pesticides, especially when their numbers are low:

By using three evaluation factors - (i) pesticide exposure, (ii)
  physiology and (iii) life history - a taxon-specific pesticide
  exposure risk factor (ERF) was created. The results suggest that about
  half of all evaluated species, and thus at least 1/3 of all European
  species exhibited a high exposure risk. Previously the region would
  have been host to a very tall high growth forests, because of the high
  temperatures, available water table of the area and fertility.

you can check pics 6 and 8 from this page to see the productivity of the region. It suggests that the reptile biomass was replaced with obese humans.
That forest has been reduced to the swamp forests where the roots are covered in stagnant water for most of the year, where some large aquatic reptiles take refuge, and which is completely different than the lost forests of the Mississippi plains.
The old forests would have perhaps been similar to florida's inland forest, and perhaps very different, because of the available water table, and much more productive silt, than florida's ground allows for. I didn't manage to find photos of the lost forests of Mississippi plain regions, they would have been dense, producing 3-7 times more biomass than normal forests.

I agree that's an appealing explanation, but it doesn't seem to explain the lower reptile abundance in the Mississippi delta where there is less agriculture, nor in southern Florida and eastern North Carolina where there is high agricultural production but no correlated reduction in reptiles.

Did you compare the regions using the maps? at least half of florida is untended by humans, compared to 10 percent of the the Mississippi plains. only 10 percent of Florida is an agricultural plain, compared to 85% of Mississipi plains. North carolina is not an agricultural plain, check the map, none of the fields are grids, and all the fields are within 1 mile of significant amounts of forest, and only 50pc of the land is agriculture.


text:
Mathematical model for malaria
The simplest malaria model is as follows:
$$\frac{dI}{dt} = \frac{\alpha \beta I}{\alpha I + r} (1-I) - \mu I$$
where $r$ is the natural death rate of mosquitoes, $\mu$ is the death rate of humans, $\beta$ is the transmission rate from infected mosquitoes to susceptible humans, and $\alpha$ is the transmission rate from humans to mosquitoes. However, for $I \ge 1$, $dI/dt$ is negative. Wouldn't that imply that the infected class is always shrinking from the start? How does this make sense?

What is I? Overall infections?

Yes, $dI/dt$ is the rate of change of the infected population.

Where did the model come from? I'm thinking hard trying to figure this out, maybe a bit more background could help.

Martcheva, Introduction to Mathematical Epidemiology.

I am afraid you may have to read your textbook more closely. The question on page 29 states that this equation models the proportion of infected humans. If $I$  $≥1$ that would mean that there are more people are infected than there are people in total - e.g. 3/2 of people are infected - this clearly doesn't make sense.
Thus $1≥I$ when using this model.

Ah, thank you very much for clarifying. You've spared me much frustration!


text:
If human proteins are synthesized from only 20 different amino acids, then how can there be such variety of proteins in human cells?
I know that human proteins are synthesized using only 20 different amino acids. However, how can there be thousands of different proteins in human cells, if we only use 20 amino acids to make them?

because of length of proteins. for 100 amino acids long protein there are 20^100 combinations, roughly 10^130

There are only 26 letters in the English language, and more than 80% of words are under 10 letters. Yet there are over a million English words. Nonsense words don't count.
Now imagine the possibilities of a 20 letter alphabet, where the average "word" length is about 375 letters, and where words of up to 800 letters are possible. And that also does not include "nonsense words".
That should give you an idea of the possibilities, and why "thousands of different proteins in human cells" can exist.
How big is the “average” protein?

Heck, DNA and RNA use only five nucleobases (and individually only use four), and look at the possibilities there. And basically all modern computers use only two symbols to represent their state, yet we can encode pretty much anything we want with those two symbols (as long as we use enough repetitions).


text:
Comments on Experimental result regarding Anti-Bacterial soap
After using soaps, we rinse our hands with water.
Do bacteria from the water attach themselves to our hands again?
If we wipe our hands to cloth after washing our hands, do bacteria from the cloth also attach to our hands?
Or, do antibacterial substances remain on our skin and, in a sense, 'protect' us from bacteria in a given amount of time?

These are at least two different questions. Some antibacterials used in sanitizers remain on our skin for a time; others (like alcohol) just evaporate. In general, though, they don't protect us from bacteria we will encounter, but rather are formulated to destroy pathogens already on our hands so that we don't then transfer those pathogens to others or to the useal entry points on ourselves (e.g. eyes.)

Additionally: Bacteria belong to the surface of a healthy skin. This is perfectly normal, so you usually need only normal soap.

Chris's comment above can't be emphasized enough. Regular soap is enough to remove dirt and other contamination from our skin, which is where pathogens often are. Anti-bacterial compounds are not needed, as the contaminants are physically removed from the skin with appropriate washing techniques. The artificially-created hype about having to "sanitize" and "disinfect" everything is nonsense - bacteria and viruses are on and around us all the time. Overuse of substances like triclosan just lead to the build-up of antibiotic-resistant bacteria in the environment.

After using soap, the pathogens that were previously present in hands are removed by the soap and water. But yes, bacteria from the water do attach themselves to our hands again, for that we should wash our hands with clean water, which may not be sterile but at least free from pathogens. Also if we wipe our hands to cloth after washing, the bacteria that may be present in the cloth adhere itself to human hands. The attachment of bacteria depends on the concentration of microbes, increase in microbial count increases the probability and risk of contamination. Unfortunately antibacterial soaps that use triclosan may kill more microorganisms while washing hands, but then they can't "protect us" from bacteria for some longer periods of time. Also it has been found that antibacterial soaps have the potential to create antibiotic-resistant bacteria, and some may even cause allergies.

Do bacteria from the water attach themselves to our hands again?
Yes if the water does contain bacteria. Also, the chance that your hands will get contaminated is directly dependent on the concentration of bacteria in the water.
If we wipe our hands to cloth after washing our hands, do bacteria from the cloth also attach to our hands?
Same as with the water, if the clothes do contain bacteria when you touch them your hands get contaminated!
Or, do antibacterial substances remain on our skin and, in a sense, 'protect' us from bacteria in a given amount of time?
Unless you are talking about some specific fancy soap, the answer is NO, washing your hands with common soap will wipe out most (not all) of the bacteria from your hands but it will not give you any long-time protection against them.


text:
How does the mutualism of figs and wasps exactly work?
I have just rudimentary knowledge about the mutualism of figs and wasps and would like to know how this works step by step.
Also how do humans use this mutualism? Do they support or hinder it at some points?

might help to define "mutualism" and add some links so that others can follow your question...it would definitely strengthen it

@Aspergirl89 As the question stands, It is unlikely that you will get a satisfactory answer. I think it would help a lot, if you worked on your question instead of offering a bounty. Give more information what you already know about mutualism and then be more specific in what additional information you need.


text:
Recommendations for an exemplary presentation of statistics related to preclinical drug studies and cellular chemistry?
I am reading Nature's recommendations for collecting and presenting statistics, but would like to also read a few exemplary articles with good charts and data presentation to learn what it looks like when done well. Would be grateful for recommendations -- thanks!


text:
Is there any clear relationship between physical characteristics and patterns in the genome?
Given that for example humans have five fingers on each hand, is there a region in the genome with a sequence of five similar subregions, one for each finger? Is the region on the genome that encodes for the right hand near another region that encodes for the left hand?

This kind of question is what developmental genetics is all about. The answer turns out to be, in general, 'no'. There is no neat mapping between spatial dimensions of an organism and its genome. (There is one exception to this in some organisms called the Hox cluster, but they are kind of a freak case).
The reason for this is that in general you should think of the genome as being a recipe for a developmental process, rather than a description of the end product. You might have, say, a specific set of genes which is active in all limb buds, which are the structures that become limbs and fingers etc. These genes would be active at different levels, at different times and places, in your different fingers. E.g. length of time one gene is on could control how long the finger grows for and thus how long it gets.
There are some genes which are only active in specific parts of the body, but you don't necessarily need a particular set of genes for each distinct finger/limb etc. And these genes certainly don't need to be in the same place in the genome. Your left and right hand are going to have identical gene expression for instance.

Thanks. I am in general interested in how close software is to the recipe you mention and if modern software approaches are very different whether we can adapt what we learn about genetics to developing software.

In general I would say, software code is very, very different from the genetic code, because it has an intelligence behind it. Consider the difference between a road from a mountaintop to the sea, and a river making the same journey. The road's path will be far simpler and more efficient, because the stream can only follow local minima, whereas the road is designed by an intelligence that can consider the whole problem at once. Evolution can be used to generate code, but expect the results to be... different, from what a human mind would produce.

i think there are some deep questions here. but as i said, even if very different or because it is, we might learn from it.

Possibly - presumably you're aware of evolutionary algorithms. It's an active topic of research.

Yes but this may end up being very different than a programming language that uses "approaches" that nature uses to build/regulate organisms.

Fair. I guess taking natures approaches and improving on them is something we've been doing for a while. If you're interested in the nitty gritty of how gene regulation works in development, this  is a classic text on the topic.


text:
Why PCR primers don't amplify beyond the target region?
I have been doing PCR for a while. I spared a bit of time to look it up but could not find an answer. So, for sanger sequencing, if we have a primer, it can amplify about 800-1000 bp. But, if you design a set of primers (forward and reverse) for PCR it will just amplify the target region. How does DNA synthesis from the forward primer stop when it reaches the point where the reverse primer is? How does the other primer which is binding to a different strand can stop the DNA synthesis in a complementary strand?

They don't stop replication. It's just that you replicate your dna in a number of cycles, let's say 30. after which you'll have a approximatly 10^6 molecules of the amplified region and only a few longer strands.
If you draw it out you'll see that your region of interest quickly start to dominate.
original strand
----/  /----ppp-------------------------/  /--
----/  /-----------------------qqq------/  /--

after one cycle
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

after two cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

after three cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

after four cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

etc.

How does DNA synthesis from the forward primer stop when it reaches the point where the reverse primer is?

Briefly, it doesn't. You get a lot of single-stranded long pieces of DNA (step 1 here, notice the overhang ends). But the exponential part of PCR only amplified common overlapping regions in these long single strands, also known as your target region between Fwd and Rev primers (step 3)

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text:
Using degenerate primers for barcoding
I want to add DNA barcodes to the gene of interest (GOI) to identify a variant that yields high expression in neurons. I am planning to add barcodes to the 3' end of my gene so that I can use barcode counts as a proxy for counting GOI mRNA transcripts. My question is, can I use a degenerate primer with a well-defined handle to add random barcodes to my GOI? I saw some papers where they commercially synthesized barcodes. I understand that commercially synthesized barcodes have an advantage in that they would know the diversity beforehand, but it is also expensive. So, does anyone know if I can use degenerate primer for adding barcodes by PCR instead of synthesizing millions of barcodes? My forward primer will bind to the 5'end of my gene of interest, and the reverse primer will be something like this: 20bp 3'end specific sequence of GOI-degenerate nucleotides- a handle (Eg. AGCGTGGACGCTGATTCCAG-NNNNNNNNNNNNNNNNNNNN-GCCATGGCAGCTTGCAGA). Has anyone used this type of strategy for barcoding DNA ? Will this work?

I'd guess (and it is a real guess) that you won't get true barcoding because you don't know if one or more of the primers are the same in the pool that you get from the supplier. The commercially synthesized ones you know the proportions of each in the pool a priori, but your plan you don't.


text:
How much damage is caused by smoking 2-3 cigarettes on a healthy body?
I do not know how bad does 2-3  cigarettes on the average healthy body.
I do not want to include genetic factors on this issue.
So, maybe there is a study or something on this topic.
Does it cause a real damage, or to this quantities the body recovers.

2-3 cigarettes a day/week/year/life?

2-3 a day, right

I think it's suited for both of them, but i'll address it there as well.

http://tobaccocontrol.bmj.com/content/14/5/315
2-3 cigarettes could make difference absolutely.  It deals 5 points of damage exactly; just kidding.  Hopefully this study provides some insight.


text:
Does apoptosis occur more at a particular time of day?
I am interested to know if apoptosis (programmed cell death) occurs more frequently during daytime or nighttime hours, e.g. if apoptosis is associated with a circadian rhythm.
A simple search turned up a couple of articles:
Diurnal variations in the expression of radiation-induced apoptosis
The Circadian Clock Controls Sunburn Apoptosis and Erythema in Mouse Skin
However, I'm not sure how to interpret these and would appreciate the help of a biologist. I don't have a very good idea of the limitations of our investigative tools, or indeed whether my question is well-formed. Thank you!

Your question is quite well-formed, however all I can say so far is: I don't know. Maybe it is known, however I could not find any information on this in the literature. In general, little is known about the crosstalk between circadian rhythms and apoptosis. It is known that circadian rhythms regulate DNA damage repair, so I would assume that the same is true for other maintenance functions such as apoptosis of redundant or damaged cells.
I don't know which research tools are available to you, but if you want to look at the effect of the clock on apoptosis signalling in a simplified setting, I would recommend synchronising the clock of culture cells with dexamethasone (you'll find a lot on that in the literature) and then using the apoptosis read-out of your choice on samples of these cells taken in regular intervals. I recommend taking samples every 4 h over the course of 24-48 h. You can make this less tedious by synchronising separate batches at different time points. As read-out for apoptosis I recommend Caspase-3 / -7 activity, ideally by Western Blot or an enzymatic activity assay using Ac-DEVD-AMC or something similar.
If you want to have a look at the effect in a more complex, physiological model, you will have to use mice.
I hope I could help you a little. Good luck!


text:
Can anyone help identify which insect is this?
I know this may not be the right forum for insect identification, but I couldn't find any reliable source of information. Please bear with me

The insect was found on my front door, total length may be about 2 rice grains
You can see wings and slender legs behind the body
I live in India, if it matters.

I think @picapica is correct. According to this website, there are about 126 species in India, and you can narrow your search down by checking which genera & species occur in your biogeographic sub-region of India. If you happen to encounter Ephemeroptera again, and want a species-level determination, I would suggest you try to get a photo against a lighter background. The veins on the wings should be visible, as they are important for determination.

I think this is some species of mayfly (order Ephemeroptera). There are some 3000 species in the world so I can't be more precise than that. It looks very pale and it's got a bit of a strange posture, so I'm guessing it just emerged from it's larval skin (in that case the skin should be left behind close by).


text:
Continuous EEG: Where does pronounced power peak at 38 Hz come from?
I'm pretty new to EEG analysis. I measured EEG on six scalp positions over night. When I plot the power of the frequencies, I get the following:

What I want to explain (and didn't manage to) is the origin of the 38 Hz peak in my case.
The most important steps to arrive at my graph were (using Python-MNE):

band-pass filter of data (1 to 45 Hz)
resampling from 512 Hz to 200 Hz

Then for every of the six channels:

cut recording into consecutive segments of 2 sec duration

exclude segments if:

maximum allowed voltage step of 50 µV is exceeded
activity is lower than 0.5 µV
maximum and minimum amplitude exceed +/- 200 µV
maximum absolute difference of values in the segment > 200 µV

further:

retain only segments that are ok for all electrodes
randomly choose 15 such good segments (all electrodes) from every participant
calculate FFT for every 2 sec time segment for every electrode and participant
calculate mean of all these FFTs
plot

My question is: is someone familiar with such an artifact at 38 Hz? Where could it come from? These are the things I already checked:

it is pronounced in every participant
it is pronounced in every electrode
eye movements are unlikely since this peak is there after filtering out horizontal eye movements via ICA
electrical devises are unlikely since they should peak at 50 Hz
it is pronounced when segments are 6 sec instead of 2 sec
I also used a notch filter at 50 Hz instead of the bandpass filter, with the following result (here the individual 15 segments are shown, but the 38 Hz peak is still there):

Does someone have an idea where this feature could come from?

Someone taught me how to make a more informative plot without preprocessing the data. It thus seems like this artifact is 12.5 Hz apart from 50 Hz and therefore has something to do with the line noise from nearby electrical devices. The same pattern happens at 150 Hz.


text:
Photosynthesis in oxygen free enviornment
If a plant is grown in an oxygen free enviornment would it live longer in light or darkness?
It is evident that oxygen would compete with carbon dioxide during various processes like competing with carbon dioxide for reducing power, also oxygen quenches the excited electron of chlorophyll etc.
But all these effects to me don't give any sense of the extent of oxygen on these reactions. What does the absense of oxygen have on the system? Except ofcourse the plant not being able to respire properly.

So, what's your doubt here? Plants are dependent on oxygenic respiration for ATP because they evolved that way.

My doubt is which environment would the plant live longer, in light or in darkness?


text:
Can someone donate antibodies?
Consider the following scenario:

Person A has been infected with some virus (for example, SARS-CoV-2)
Person A has recovered

From this scenario, I assume Person A has managed to develop antibodies for SARS-CoV-2. If so:

For how long, after recovery, would Person A have antibodies for the virus running in their blood?
If Person A donates blood to Person B, would Person B have better responses against the virus, by using  the antibodies received along the blood from Person A? (assuming the donation is successful without issues)
Is there any paper / study building upon this idea for combating SARS-CoV-2?

Notes:

I am not expecting exact quantitative answers to these questions. I just want basic understanding for reasons this could or could not work.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. I therefore think  that your question on dealing with the coronavirus outbreak is off-topic here. You are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Sorry about that. Is there another SE in which this topic would have been more appropriate? Also, I have to point out that your comment about SE being "not a discussion site or a site for floating ideas" is also off-topic, since I know that very well and did not call for any discussion and asked directly answerable questions, to which in fact I answered myself.

You could try SE Medical Sciences. However there is a very good article in today’s Financial Times (27 March) on the subject. I’m a subscriber to the paper edition, but you may find it on line. You’re probably entitled to three free articles. If you are not familiar with the FT do not be put off by its name. It is the foremost British serious newspaper (with US and European offices). In times like these you need to know where to find reliable information.

@David Thank you!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. In addition, each of those questions must be appropriate for this site! ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Does this answer your question? How does the body respond to blood donation; are there any possible risks?

Question 1

[...] antibodies [...] can last anywhere between a few weeks to a few months. The antibodies themselves though (which are proteins) definitely don't last forever (like all proteins). Eventually certain suppressor cells kill off plasma cells after the response has taken its course, and all that remains are a few memory cells, which are reactivated again should the pathogen invade the body in the future.

Source
Question 2 and 3
Yes.

Here is an article from Johns Hopkins University.
Here is a paper by Arturo Casadevall and Liise-anne Pirofski mentioned in the above article and published on the Journal of Clinical Investigation on March 13, 2020.

Fun fact: I was about to say in the question that I tried to research but didn't find anything. But I decided to make a last attempt, and actually found the answers...

Please note that while answering your own questions is completely fine, you should first fix (where possible) and/or delete the problematic sections of your question. ——— In addition, link only answers (what you provide for your second and third questions) are not acceptable — answers should not require other users to follow links (links also often break rendering the answer completely useless in the future). Please consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


text:
Interpreting Allele frequency and allele count
In the following vcf file, the AF allele frequency of ALT allele  is 1.0. Does it mean that it is not a true SNP of interest? Does it also mean that ALT allele always occurs and REF allele never occurs in the population?
Also not sure how allele count AC=37 is being calculated.
Chr1 pos=565286, REF=C, ALT=T, Info AC=37; AF=1.0 Format GT:AC:AF:NC Child=1:11:1.0:+T=4,-T=7 mother=1:26:1.0:+T=8,-T=18,
Cheers,
Ambi.

Please let us know a bit more about your .vcf file. Spontaneously, I would say that all individuals in that file have a different allele (ALT) than the human reference (REF). It"s impossible to give an interpretation based on these information though. Allele count is defined as: "AC : allele count in genotypes, for each ALT allele, in the same order as listed" in the .vcf specification file. It is not really calculated, it is counted.


text:
Spores bacillus subtilis in milk
I need to inoculate spores into milk and then count on the plate. I never see a spore, so how i recognize it from the germ cell? does anyone know the procedure and if there are differences from a normal count in agar colonies?

If you need to inoculate milk with a known number of Bacillus subtilis spores then you will have to go follow a "sporulation" protocol - (going by your question I am not 100% certain whether this is what you want to do).
However, please find a sporulation protocol, developed by the Universities of Bonn and Freiburg, below:
Sporulation

Overnight culture

Inoculate your culture of Bacillus subtilis in 4 ml LB-medium
Let them grow overnight at 37°C, 200 rpm

Exponential growth

Measure the OD600 of your overnight culture and dilute it in LB-medium to an
OD600 off around 0.1-0.2/ml in 10 ml LB
Let the cells grow to an OD600 of 0,8/ml (37°C, 200 rpm)

Sporulation

Centrifuge 10 ml of the cells at 13,000 x g for 1 minute
Wash the pellet with 1 x PBS
Re-suspend the pellet in 5 ml DSM (Difco Sporulation Medium)
Let the cells grow for 24 hours at 37°C (200 rpm)

Lysozyme treatment (additional for spore purification)

Treat the samples with lysozyme (15 mg/ml) at a dilution of 1:6
Incubate for 1 h at room temperature
Wash 6 times with 1 x PBS

Additional:

count spores using a Neubauer improved counting chamber and make aliquots
with a defined number of spores per aliquot (e.g. 100 Million spores per 500 μl)

(Note: always use fresh DSM since the FeSO4 is rusting when it is in dilution)
May I make special mention of the Bacillus subtilis Manual here which was put together by the iGEM team and has proved as an excellent resource. The protocol above was taken from it.
Once you have your spore counts you can then inoculate the milk to your liking. However, please be aware that milk, unless completely pasteurised prior to inoculation, is not a sterile product. This means that other organisms might grow on whatever agar you decide to plate out on.

Thank you, but i have already a culture of b.subtilis spores (10^8), i have only to put into milk. Then this milk (+spore) will be treated (temperature etc) to try to kill the spores. After treatment i have to.count how much we have reduced the number of spores. I put 1 ml for inclusion in petri plate with pca+skim milk. Now, how i count spores? As a common colonies? Or are different? If there are spore and germinative in the same plate how i recognize spores?

Ah, OK. I'm with you now @StarChips. I don't think there's a way to detect spores as such on agar plates. They are easy to small. You would rather operate on the assumption that all the colonies that you can see on your PCA plates stem from spores. Given that you only inoculate with spores. So at the end you just count the colonies.

Yes, but i don't know if the condition of treatment could cause sporulation. I want to be sure to count only spores

Chances are that the treatment will cause sporulation given that some live, vegetative Bacillus subtilis cells are present in the sample. If you really want to be 100% certain that all you count are spores or colonies from spores then you have to go through far more effort. This can't be done on agar plates only. Unfortunately this article is behind a paywall but in its abstract it outlines a wee bit what is required to get an accurate answer on spore counts in your sample: http://www.sciencedirect.com/science/article/pii/S0167701211003526?via%3Dihub