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Is there evidence that children should play in dirt to get healthy?
I've heard it said many times, that we should let children play in the dirt as it builds up their immunity and prevents things like allergies in later life.
I have another suggestion which, to me, is equally plausible. In older times when families had lots of children, and they used to play in the dirt, those weaker children used to get ill and die. Leaving the `stronger' children who were less suceptible to allergies and diseases to grow to adulthood.
So in our cleaner lifestyles where we prevent our children from playing in the dirt, actually we are just letting children who would normally have died off early grow to adults. (Which is a good thing from a moral standpoint - although overall it means the human population as a whole grows weaker in the short term).
Therefor telling people to let their children play in the dirt is bad advice if this is true.
Which of these two options do you think is the truth?
(Mathematically, let us assume that by random chance 50% of babies have bad immunity, but that parents have an average of 4 children. This means if half the childen die in childhood, the adult population would be full of people with good immunity. This is my terrible conclusion which has no moral solution.)

This answer focuses primarily on allergies, for which there is more reliable research, but touches on general immunity towards the end.
It is certainly true that the prevalence of allergies is increasing worldwide, and seems to be related to a rise in the so-called 'modern lifestyle' which avoids exposure to potentially harmful environmental factors.

The prevalence of allergic diseases and asthma are increasing worldwide, particularly in low and middle income countries. Moreover, the complexity and severity of allergic diseases, including asthma, continue to increase especially in children and young adults, who are bearing the greatest burden of these trends. - World Allergy Organisation Journal

The idea that playing in the dirt builds an individual's immune system and reduces the chances of allergies etc. is known as the "hygiene hypothesis" (or, more accurately, the hygiene hypothesis states that

due to reduced exposure to microbial components, the proposed allergy-preventing potential of these factors is no more present in sufficient qualities and/or quantities, which leads to an imbalance of the immune system with a predisposition to the development of allergic disorders." - Epidemiological and immunological evidence for the hygiene hypothesis.

)
Aside from potential mechanisms, there is certainly evidence for the hygeine hypothesis

The researchers studied the immune system of mice lacking bacteria or any other microbes ("germ-free mice") and compared them to mice living in a normal environment with microbes.
  They found that germ-free mice had exaggerated inflammation of the lungs and colon resembling asthma and colitis, respectively. This was caused by the hyperactivity of a unique class of T cells (immune cells) that had been previously linked to these disorders in both mice and humans.
  most importantly, the researchers discovered that exposing the germ-free mice to microbes during their first weeks of life, but not when exposed later in adult life, led to a normalized immune system and prevention of diseases.
  Moreover, the protection provided by early-life exposure to microbes was long-lasting, as predicted by the hygiene hypothesis. - Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function

As far as I know there is no consensus on this issue, however a number of scientific studies have proposed potential mechanisms to explain the rise in allergies and other such conditions; one of the most widely accepted ideas is that an avoidance of germs and microbes early on in life leads to

changes in the fine balancing of T helper cell 1 (Th1), Th2 and regulatory T cell (Treg) responses which are triggered by altered or missing innate immune cell activation. In fact, proper activation of cells of the innate immune system via their so-called pattern recognition receptors has been demonstrated to play a crucial role in early shaping of the immune system and suppression of the development of Th2-driven allergic immune responses. - Epidemiological and immunological evidence for the hygiene hypothesis.

this would seem to explain the observed phenomena.
It is definitely true though that there has been and will continue to be an element of natural selection involved here, as you have pointed out, because it is a force that is found pretty reliably in these sorts of situations. It is certainly logical that exposure to microbes during infancy will help weed out those with a weaker immune system (assuming they died because of infection/disease etc.), which over time would create a population and species that was more resilient. However, I can't find any studies to back up this idea. It is also a somewhat separate issue to the idea of the hygeine hypothesis, which describes changes to a specific individual within their lifetime rather than necessarily across a population due to natural selection and evolution, which is the explanation you have provided (unless I misunderstand your point?).
I only have a general understanding of immunity, however it is generally accepted that exposure to a pathogen (if this episode is survived) will result in an immune system which is better able to counter that pathogen in the future - this is the whole concept of vaccinations. therefore it makes sense that, again, low levels of contact with 'germs' will build a child's immunity.
Overall I think that it is a complex issue without a generally accepted answer as yet, however it seems to me based on this research that "playing in dirt" (in other words, being exposed to low levels of pathogens, microbes and toxins) does in fact build immunity and reduce the likelihood of developing allergies in later life, even if we don't know the exact mechanism for this yet.
aside from any potential immunity benefits, most children find playing in dirt fun (I know i did), so for the most part i'd say let them do it anyway!
My sources:

https://www.sciencedaily.com/releases/2012/03/120322142157.htm
https://www.ncbi.nlm.nih.gov/pubmed/17544829
https://waojournal.biomedcentral.com/articles/10.1186/1939-4551-7-12

Thanks for your answer. I didn't mean exactly natural selection in the terms of evolution over a long time. I meant really in terms of it may be "natural" for a human to have 4+ children and for only the strongest to survive each generation. And that all through human history perhaps women have always had half their children with bad immunity. So my suggestion is that this is nothing new. Even those with bad immunity, their children may have half-good and half-bad immunity. So I'm not saying immnuty is passed on by any means, more that is is just random at birth.


text:
Are there poisons that affect only mammals but not reptiles
Are there poisons that affect only mammals but not reptiles or crustaceans?
E.g. hemotoxins which affect hemoglobin but not hemocyanin or specific Na+ channels?
Looking for a "nice" poison/disease as idea for a fictional story to explain survival of reptiles/crustaceans vs. mammals.

"Reptiles" are not very different from mammals (compared to crustaceans).

Good candidates would likely be poisons originating from reptiles/crustaceans themselves...

source: Stack Exchange

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

sort: votes


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Is this a Zelus luridus?

I found this little bug on my bed and I got curious to know what it was, I did some researches and then I noticed that it is very similar to Zelus Nymph but I can't be sure of it. Can you confirm it?
Here is a processed version of the image:

I'm sorry to say we still need a better picture; the focus (or rather lack thereof) makes any identification suspect (though looking at the front pair of legs as-is makes me suspect that any Assassin Bug identification is likely wrong).

Ok, thank you for the comment. If I can I'm taking a better picture.

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


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Do lychees cause encephalitis?
In India, there is a recent outbreak of this disease after many consumed lychees.
Many people link this to lychee's "toxins".
I'm not a biology major hence can't elaborate further on this, but here are some links.
Link 1
Link 2
Here is another that claims that lychees must not be consumed empty stomach .
Link 3

There are many articles on this topic (including many intended for laypersons). Did you even try to read the articles carefully, that you yourself mentioned? I'm voting to put this question on hold because I don't even see a question here.

@WYSIWYG the studies are published by the newspapers, which in general shouldn't be considered reputable . I only asked here to verify if there is an actual scientific evidence for this.

Your second link is an article in Lancet, a highly reputed medical journal.


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Unusual terminology of vector used
What is the significance of a+ in the name pET-28 a(+)? Is there any a- strain and differences between a,a+,a-?

This is not a bacterial strain. pET is a plasmid system generally used for protein overexpression. If your stocks are labelled like this then you should ask the person who created them.

There are 3 versions (a,b, and c) of this plasmid with different multiple cloning sites.
You can safely ignore the "(+)" part unless you are packing your plasmids into viruses.
You can learn about the details and see sequences from the resources available on the Millipore website.  I found this by searching for "pET-28 a(+)" ...


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A theoretical ethical dilemma
For all those who keep in touch with advancements in field of biology iPSCs ought not to be a foreign term. iPSCs are now being used to make organ models to be able to study diseases and how drugs will affect them without needing any living host. I expect this organ modelling to become more and more advanced in future and soon all complete organs to be made using this technology. However should making a complete living brain ever be allowed for studying diseases as we are mostly our brain, so maybe while using such living brains we are making conscious systems on which we are experimenting?

Consciousness and the brain are two different things. In-vitro grown brains would have no memories, no experience and thus no consciousness. It's like a computer without software. Plus, animals we are using now in science like rats, mice and other mammals are conscious already. Where is the dilemma?

Yes you are right in a way. But then when anything that becomes anything comes even close to human consciousness the moral obligations increase many folds. So it becomes difficult for me. Thanks for your answer.

I agree that iPSCs will continue to be developed and will probably be used to make brains at some point in the future. Whilst it's obviously not possible right now, feasibility isn't the issue here. A lot of my answer will be somewhat opinion based as a result of the nature of such an ethical question.
As to the ethics of experimenting on such living brains, It's undeniably a tricky question - and, as with all ethical dilemmas, suffers from the inherent variability of ethics and morals (you will struggle to find two people with exactly identical ideas about right and wrong, and from a purely logical and scientific perspective there's no reason to believe that moral objectives exist at all).
An interesting phrase that you use in your question is "we are mostly our brain". I suppose it depends on what characteristics you're looking at: a brain alone would be incapable of surviving and by mass the brain only accounts for around 2% of the human body. we are mostly water; simple, lifeless and unconscious.
Therefore we are evidently ranging into territory of consciousness, and by "we" you are referring to our seemingly conscious 'mind' as conjured by the complexities of the brain. As for this, I think perhaps the philosophy stack exchange is the place to go...
Ultimately it depends on whether we look at a brain as simply a collection of atoms which form molecules, cells, tissues and then organs or as something more - this is the whole idea of emergence (for example, an individual ant is unconscious and negligible, but many thousands of ants communicating using chemicals and simple commands forms a highly complex and adaptable ant colony - the ant colony is greater than the sum of its parts). if the former is true, then there should be no difference in manufacturing a brain and experimenting on it to making muscle tissue and performing experiments on that (or even creating a crystal from chemicals and using that for experiments). If we look at the brain as something greater than the simple sum of its parts - as a living, conscious being - then I suppose we'd need to go through the proper channels that we have now when dealing with something that's alive.
From here an infinite variety of problems crop up: would the brain be given the full rights of a human, or treated more like animal test subjects? Would consent from the brain be required? Could a brain even be conscious if unattached to the rest of a body? Would killing the brain be murder as it would be with a human?
So far I've just been stating issues: my personal opinion is that we ought to find a balance somewhere between treating the potentially conscious brain as merely an impressively complex collection of lifeless components and giving it the full rights of a human being. where that line should be drawn? I don't really know. Personally, I'd rather test drugs and treatments on a mere brain than on a fully formed and functional human being, but someone else might not agree.
These questions are always difficult, and science can't really give any reasonable answers (scientists can't even agree on what makes something alive, let alone conscious). there is an entire field called bioethics devoted to things like this.
my advice would be to ask this on the philosophy stack exchange as you will get some interesting answers there.

Thanks a lot for such a well considered answer.


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Studying the epigenetic variability, can I use SNPs?
So, I'm trying to study the effects of epigenetic variability on the brain structure. Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region? I don't have environmental data, just the SNP information.
Since epigenetics refers to the variations in the gene expression without changing the DNA sequence, I don't really understand if there could be a connection.
Any help would be appreciated, thank you!

Welcome to StackExchange! If I got this right your main interest are epigenetics and brain structure, I'm not sure how SNPs play into this since they are only loosely connected to either. I think you could improve your question by making clearer: 1) what kind of data you will/can work with (data types & internal/public resources), 2) What your approach to studying this is (project time frame, dry lab / wet lab, expected readout).

Thank you for your response! :) The SNPs are basically used to compute the probability of a gene being expressed in a brain region (thalamus for example) and then correlate that with the brain structure for patients with psychosis, in my case. The data is from public databases like BrainEAC that have information about the gene's SNPs. The title of my project suggests that I'm studying epigenetic variability of psychosis but I will be using SNPs associated to gene expression to determine the expression of a gene. My adviser is not available and I needed this to proceed with my lit. review.

Starting from what appears to be your main question:

Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region?

I would strongly advise against using SNPs determine if genes are expressed (at all) in a given tissue.For one thing SNPs that affect expression (then often called eQTLs) will usually only have small +- effects on expression instead of switching it on/off and also have that effect in many/all cell types. Unless an (individual) SNP has clearly described /and validated effects on gene expression in a specific tissue/brain region, you should assume it has global effects.
Now, luckily for you gene expression in different cell types, tissues etc is a relatively well studied area and there are resources for gene expression in the brain available (brain atlas is probably closest to what you might look for).
You can uses these resources to determine which genes are expressed in your regions of interest and from there on check if SNPs associated with these genes correlate with certain structural brain features you are interest in.
One more thing you note:
The title of your questions (as well es comments) mention that you are interested in epigenetics. Neither gene expression nor SNPs/eQTLS are diretcly linked to epigenetics, so if this is your actual focus you should also look for availbale ChIP-seq data or similar and also include this into your analysis (correlation of SNPs with epigenetic marks is difficult but not impossible)

I agree with Nicolai. Epigenetic variation is usually studied as DNA methylation (usually via bisulfite sequencing) and histone modification (via chip-seq). The study of gene expression is another topic. What is your research question?


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Help with jellyfish species identification
Our research group (Evolutionary Genetics Group, University of Zurich) has received a letter from a special needs child who has kindly asked us to identify three jellyfish species.
Unfortunately, the letter does not include anything else except three rather low quality cutouts from what I assume is a childrens book. Nobody in our lab has any knowledge about jellyfish taxonomy so any help is greatly appreciated.

https://jellywatch.org/

Be warned that these are just best guesses - as you said yourself, these aren't great images for identification as they appear to be simple drawings:
1) this looks a lot like Aurelia aurita - though the lack of any internal patterning in the drawing makes me think perhaps otherwise.

image source: https://www.leisurepro.com/blog/wp-content/uploads/2017/05/shutterstock_272438348.jpg, https://holidays-majorca.co.uk/wp-content/uploads/2017/01/Aurelia-Aurita-S-300x225.jpg
2) possibly a Turritopsis dohrnii or nutricala - if so then this is the 'immortal' jellyfish. shape of bell is correct and the lappets seem reasonably close, it's just the internal structures that I'm not sure about.

image source: https://www.cairnsholidayspecialists.com.au/shared_resources/media/irukandji-jellyfish-in-far-north-18836_400x322.jpg
3) Very unsure about this one, but potentially a Atolla wyvillei? definitely has some visual features in common and I can't find anything else that's similar. I can also see how an artist would derive that image from this species.

Image source: https://www.mindenpictures.com/cache/pcache2/90194947.jpg, https://c8.alamy.com/comp/E45A4H/deepsea-medusa-jellyfish-atolla-manubrium-gulf-of-maine-atlantic-E45A4H.jpg
I hope these at least give a starting point and are of some help, I think the nature of those images will make it hard to get many better answers. Good luck!!

Thank you very much! I did get in touch with Lisa Gershwin via email as well. Species ID I got from her are: 1: Aequorea victoria, 2: Polyorchis penicillatus, 3: Atolla wyvillei. But I think based on the photo quality one cannot be 100% sure. In any case, I'm sure the kid will be excited and I will send him the full list with all species proposed.

Well, I defer to her better judgment! They certainly fit better than my ones... I'm chuffed to bits that I got Atolla wyvillei right though!

-1. Looks like your 1st 2 are wrong. Good job on the third. (You can [edit] if you think you can improve your answer)


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Why does this plum/apricot hybrid look like brains?

Why does this plum/apricot hybrid look like brains?
Notes:

Here's a photo of what a normal fruit on the tree looks like.
Location is Zone 5, east of Toronto.
There are about 20 other fruits on the tree. This the only fruit on the tree that has this problem.
The date is June 26, 2019 (although plants have been delayed by about 3 weeks this year due to unusually cool and rainy weather).
I have had lots of disease problems on my prunus this year due to the wet weather.

It is difficult to say, but it is likely due to disease. Many plant diseases have the effect of convincing plant tissues that they are some other organ than what they actually are, which leads to deformations.
I was not able to find anything that looked as dramatic as the image that you show, but there are similar diseases in stone fruits that deform fruit:

Plum pox potyvirus: http://download.ceris.purdue.edu/file/1424
Plum pocket fungus/"Bent banana disease": https://pnwhandbooks.org/plantdisease/host-disease/prune-plum-prunus-spp-plum-pockets, http://shropshireprunedamson.com/a-bad-case-of-bent-banana-disease/

I hope that this is helpful.

Another search term that might help or interest the OP is "gall" which describes such "fooled" tissue growths. https://en.m.wikipedia.org/wiki/Gall

This is a guess, but perhaps the result of an infection by a fungal plant pathogen related to Taphrina deformans. T deformans infects species of the genus Prunus (i.e. the genus of prunes and apricots), but it's best known for causing peach leaf curl in another Prunus species, peaches.
For example, see this image of T. deformans infecting a leaf in Catalonia, Spain:

 Source: flickriver; Credit: esat_ahi
From Wikipedia:

trees infected with T. deformans will experience leaf puckering and distortion, acquiring a characteristic downward and inward curl. Leaves will also undergo chlorosis, turning a pale green or yellow, and later show a red or purple tint

And guess what? According to Wikipedia:

The fungus has higher infection rates following cooler, damper winters.

Are you sure your infected plant part is a fruit and not a grossly infected leaf? (Did you cut open the infected fruit to examine it closer)?
Management:
If it is T. deformans, Wikipedia summarizes some good management strategies:

Because infection depends on a wet environment, appropriate irrigation of crops can help control pathogen dispersal. Although some sources also suggest thinning fruit to control the spread of disease,[3] sanitation and culturing practices alone are insufficient to manage the pathogen.[2] Fungicide is preferred; chlorothalonil and ziram are favored, and copper is an organic option.[4] Fungicide application requires the correct timing and complete coverage of the crop.[11] It is recommended that growers spray fungicides after leaf-fall, or after 90% senescence of leaves. In wetter climates, where multiple sprays may be necessary, spraying is recommended in the late fall and in late winter or early spring.[3] Post-infection spraying of fungicide is inadequate to control the disease.[11]

Update: (Side-note)
I still think T. deformans seems like a possible cause of your plum disease, but...
Apparently, there is a closely related species to T deformans called Taphrina communis, which causes Plum pocket by instead infecting the fruits of plums.

According to Kansas State University Research and Extension:

In contrast to peach leaf curl, symptoms of plum pocket are most conspicuous on the fruit. Small, whitish spots develop on young plums soon after blossom. The spots enlarge and eventually cover the entire fruit. Seed fails to form in infected plums; the fruit becomes hollow and enlarges to many times normal size. At this stage, the distorted plums have a red to grayish tint. Young shoots and leaves may be deformed and killed by the disease, but these symptoms are not as common as in peach leaf curl.

I couldn't find any pictures that matched your tree's symptoms, and truthfully the symptoms of plum pocket don't quite match what you're describing. However, for completeness sake, I thought I'd add this information here.


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Definition for different arrhythmia
I am wondering if there is an organization, a document or a research that standardize all the rhythms? Such as describing how long should the ECG be flatline to be considered as asystole? The rhythm I am focusing on is:

Asystole
Missed beat
Tachycardia
Bradycardia
PAC
PVC
Bigeminy
Trigeminy
Atrial Fibrillation

Basic Cardiac Rhythms – Identification and Response (The University of Toledo, Medical Center)
This quite thorough one-page source describes:

Basic heart anatomy and physiology
The meaning of the waves in ECG
Examples of ECGs for most arrhythmias with timing, causes, symptoms and treatment

Here's Pocket Guide to Neonatal ECG Interpretation (NICU INK Book Publishers) - an one-page source about arrhythmias in infants.


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How far can parrots fly without needing to land?
This is for a story I'm writing.  I can't find any information on how far various parrot species can travel without needing to land-- the closest I could find is this page saying that a macaw flies up to 15 miles looking for food.  Intuitively I would think that larger birds, like macaws and African greys, would be able to fly farther than smaller ones due to having stronger wings, but the nonstop-flight record-holder is about the size of a robin so I guess that's not necessarily true.
Can anyone tell me how far various parrots can fly in a stretch, or at least the farthest that any parrot species can fly?

related https://biology.stackexchange.com/q/23530/3340

@David. This site is open to anybody that wishes to use it. The OP clearly is asking a biological question which is on-topic here. It doesn't matter what their end-use of this information is. Please review our on-topic guidelines and our Code of Conduct. Most importantly, be nice to new users!

@theforestecologist — OK, then it’s off-topic because he should have done his own research. I know nothing about parrots (other than you’re not supposed to shoot them in Australia) but was able to find an answer in a few minutes googling (at parrot.org). The site is supposed to be for serious students of biology and I think this sort of question is too like a Guinness Book of Records question.

@David Could you provide a link?  I haven't been able to find an answer to this, and parrot.org doesn't seem to be at all related to my question.

The page I found was https://www.parrots.org/ask-an-expert/comparison-of-flight-mileage-for-various-wild-parrot-species. It is a bit iffy in that some of the figures are miles per day (presumably landing in between) but others are non-stop between islands. Probably not as much detail as you would like, but a start. I searched for "range of flight of parrots". Another problem is that there is a drone with the name "parrot" so best to use plural.

@David this is actually a legitimate question: "What is the max/average flight duration of ___ species of bird?". Unfortunately, proper references are available only for some few selected species of migratory birds.

@WYSIWYG — See my response to theforestecologist. Ironic that I'm the only person that has provided anything.

Birds of flight were the original inspiration for the design of a machine that could fly and carry a person aloft, hence it's not surprising that the aerodynamics of avian flight and aircraft have much in common. Specifically, they both consume mass as the source of energy to maintain flight; jet fuel or gasoline in the case of airplanes, and stored body fat in birds, and they both have wings that provide aerodynamic lift as the air moves over them during flight. In addition, both share another characteristic of flight, the ability to glide, to continue flight without providing any of their own energy to maintain that flight. This energy is provided by the atmosphere itself in the form of rising air currents caused by a difference in temperature of a local 'pocket' of air; a pocket of air that is warmer than the surrounding air will rise because it has lower density, the Archimedes Principle in action. A similar process occurs when a parcel of moist air is surrounded by dry air at the same temperature as the moist air hence less dense than dry air. The third source of rising air is due to the local topography; the air on the windward side of a ridge or mountain is forced upward and is frequently used by birds as a source of lift.
Any discussion of gliding flight will unavoidably involve some aspects of atmospheric physics (a.k.a., weather), it's no different here. As stated above, a parcel of moist air surrounded by dry(er) air at the same temperature will rise. As long as that temperature is above the saturation temperature (the dew point) for that parcel of air, the water will remain in vapor form. We all know that as we go higher in the atmosphere the temperature drops; it's cooler at the top of a mountain than at its base. Therefore, as our parcel of moist air rises its temperature will drop, and eventually that temperature is the same as the dew point in that parcel leading to the condensation of that moisture, i.e., a cloud forms. As a surface of constant temperature in the atmosphere is nearly a level surface, we see clouds in the sky whose bases are all at the same level, the level where this condensation begins. Now, for a little of thermodynamics; when we boil water by adding heat (that is energy) to it, we are turning liquid water into a vapor (steam). Here's the thing, when we cool that steam down to the dew point it will condense back into liquid water, and in doing so, we get the heat (that was put in to make it boil) back again! That recovered heat shows up as an increase in temperature of the air that just gave up the water vapor. This increase in temperature causes that air to continue to rise, now due to a temperature difference with the surrounding air rather than a water vapor pressure difference; the cloud continues to grow upwards. This is the source of the cumulonimbus clouds we see in the sky that may eventually form thunderstorms. This discussion hi-lights a key fact about weather that relates directly to our discussion about gliding flight; if there are no updrafts, there are no clouds. That's correct, for a cloud to form, there must be updrafts containing moist air. No clouds indicates no updrafts. If there are no updrafts, there is no gliding flight. However, we note that really dry air is very hard to find; there still might be thermals around, but not likely, and those not very strong. The take away from this discussion is this: if we want to include increases in maximum range resulting from gliding flight, we need to be able to predict the weather (which hasn't happened yet, and I say this as one who has spent years as an undergraduate and graduate student active in atmospheric research.). Hence, long distance gliding flight will not be addressed any further here.
We begin our analysis of powered flight by considering a specific airplane, say a Boeing 787 passenger jet. To find its maximum range, the aircraft would be completely fueled up, take off and fly a level, constant speed flight path, as any accelerations (by changing altitude or going faster) would waist fuel. When the fuel tank goes dry, you have reached the maximum range of powered flight (assuming no head or tail winds of course).
From an analytic point of view, the fuel carried by the 787 is the source of energy, $E_s$, that powers its engines. These engines produce the thrust force, $\mathbf{T} = T\mathbf{\hat{T}}$ directed horizontally, parallel to the 787's longitudinal axis and to the flight path, that counteracts the effect of the atmospheric drag force, $\mathbf{D} = D\mathbf{\hat{D}}$ that opposes the 787's motion along its flight path. Under steady flight conditions (constant speed and altitude), the net horizontal forces on the 787 is zero so that $\mathbf{T} + \mathbf{D} = \mathbf{0}$, or $\mathbf{D}=-\mathbf{T}$. Taking the magnitude of both sides of this expression we find that $D=T$ so that $\mathbf{\hat{D}}=-\mathbf{\hat{T}}$. We find that the thrust generated by the engines has the same magnitude as, but directed opposite to the atmospheric drag.
Under the same flight conditions, we find a similar relationship for the vertical components of force acting on the 787, its weight, $\mathbf{F}_w = F_w\mathbf{\hat{F}}_w$ is balanced by the lift $\mathbf{L} = L\mathbf{\hat{L}}$ generated by the wings so that $F_w = m_p g = L$ and $\mathbf{\hat{L}}=-\mathbf{\hat{F}}_w$ where $m_p$ is the instantaneous mass (= takeoff mass of the plane, $m_{p_0}$, less the mass of fuel expended so far generating thrust) of the 787 and $g=9.8\, \text{m/s}^2$ is the standard gravitational acceleration on the surface of the Earth. We note here, that under these flight conditions, both $\mathbf{L}$ and $\mathbf{F}_w$ are perpendicular to $\mathbf{T}$ and $\mathbf{D}$.
If the thrust is removed so that $\mathbf{T}=\mathbf{0}$, then the drag force will no longer be opposed and will slow the plane down, reducing the speed of air flowing over the wing, which in turn will cause the wing to generate less lift, thus initiating the plane's descent (its weight is greater than the lift produced by the wings). If the plane is then 'nosed down' by an angle $\alpha$ from the horizontal, the projection of the plane's weight vector, $\mathbf{F}_w$ onto the plane's longitudinal axis will no longer be zero, but will instead be $\mathbf{F}_w\sin\alpha$ directed forward opposing the drag force. If $\alpha$ is chosen so that the sum of this projection and the drag vector is zero, then the plane will descend at a constant rate and the magnitude of the drag is given by $D = F_w\sin\alpha$. The projection of the weight vector onto the axis perpendicular to the plane's longitudinal axis, $\mathbf{F}_w\cos\alpha$, is balanced by the equal magnitude but oppositely directed lift vector, whose magnitude now becomes $L = F_w\cos\alpha$. If we form the ratio $D/L$ we find
\begin{equation}
\frac{D}{L} = \frac{F_w\sin\alpha}{F_w\cos\alpha} = \tan{\alpha} \tag{1}\label{1}
\end{equation}
The inverse of this ratio, $L_D = L/D = (\tan\alpha)^{-1}$, is known in aerodynamics as the lift to drag ratio while the angle $\alpha$ is called the glide slope angle. These two  parameters are important in the overall characterization of the aerodynamics of an air-frame. Once this ratio is known, it can be used to estimate the drag in level flight. But in level flight, the lift is equal in magnitude to the plane's weight, $L=F_w=m_p g$. Substituting this expression into Eq.~$\eqref{1}$ and solving for the drag
\begin{equation}
D = L\tan\alpha = F_w\tan\alpha = m_p g\tan\alpha  \tag{2}\label{2}
\end{equation}
We have reached the point in our analyses that we need to address the mass/energy budget for the plane's flight. It will be useful to separate the mass of the plane into its empty (no fuel) mass, $m_{p_e}$, and the mass of available fuel, $m_f$, with the initial, takeoff mass of fuel given by $m_{f_0}$. With these quantities defined, the initial takeoff mass of the plane is given by $m_{p_0} = m_{p_e} + m_{f_0}$ while the instantaneous mass is given by $m_p = m_{p_e} + m_f$. During flight, the mass of the fuel available, $m_f$, varies such that $m_{f_0} \ge m_f \ge 0$ while the mass of the plane, $m_p$, varies as $m_{p_0} \ge m_p \ge m_{p_e}$.
There are two additional constants required to determine the net effective energy available to do work against the drag force when consuming the (differential) quantity $\delta m_f$ of fuel while flying the (differential) distance $\delta \mathbf{r}$. The first of these, $\kappa$, determines the total (differential) energy, $\delta E$, available from the combustion of the quantity $\delta m_f$ of fuel
\begin{equation}
\delta E = \kappa \delta m_f   \tag{3}\label{3}
\end{equation}
For an American airplane such as the 787, $\kappa$ will have units something like BTU per pound of fuel expended.
The second, $\eta$, specifies the efficiency of converting the available energy into actual work, $\delta W$, generating thrust that counteracts the drag
\begin{equation}
\delta W = \eta \delta E = \eta \kappa \delta m_f = - \mathbf{T}\cdot\delta\mathbf{r} = - m_p g\tan\alpha \delta r \tag{4}\label{4}
\end{equation}
where $\delta\mathbf{r} = \delta r \mathbf{\hat{T}}$ is a differential displacement vector along the flight path during constant velocity, horizontal motion and the minus sign accounts for the fact that the plane's energy stores are consumed as that energy is used to counteract drag (a fundamentally dissipative process).
Letting the $\delta$'s become derivatives, dividing through by $m_p$ and using $m_p = m_{p_e} + m_f$ and replacing the integrated variables by primed quantities, , Eq.~$\eqref{4}$ can be rewritten in the integral form
\begin{equation}
\eta \kappa \int_{m_{f_0}}^{m_f} \frac{dm'}{m_{p_0} + m'}
= - g\tan\alpha \int_0^r dr'   \tag{5}\label{5}
\end{equation}
with the limits of integration evaluated at takeoff and the current downrange position a distance $r$ from takeoff.
Performing the integrations indicated in Eq.~$\eqref{5}$ and simplifying, we have the result
\begin{equation}
m_p = m_{p_0} e^{-\frac{g\tan\alpha}{\kappa\eta}r}   \tag{6}\label{6}
\end{equation}
We find that the mass of the plane, $m_p$, is an exponentially decreasing function of the distance flown, $r$. Letting $r=r_m$ be the maximum range of plane where all fuel has been expended (when $m_f=0$ so that $m_p = m_{p_e}$), Eq.~$\eqref{6}$ becomes
\begin{equation}
m_{p_e} = m_{p_0} e^{-\frac{g\tan\alpha}{\kappa\eta}r_m}   \tag{7}\label{7}
\end{equation}
We note the similarity of this expression to that of the Tsiolkovsky rocket equation.
Eq.~$\eqref{7}$ can be solved for the maximum range $r_m$
\begin{equation}
r_m = \frac{\kappa\eta}{g\tan\alpha}\ln\left(\frac{m_{p_0}}{m_{p_e}}\right)
   \tag{8}\label{8}
\end{equation}
an amazingly simple result, all things considered! This result remains valid for any aerodynamic system that obtains its lift via forward motion through the air provided by a propulsion system that consumes mass to produce thrust. It could be applied to a Cessna 172, or even a nitro powered radio controlled (RC) model of a 172. It could not be applied to an electrically (battery) powered model of the 172 because there is no mass loss from a battery, or to any type of glider (no thrust or mass loss). And it can, however, be applied to any bird of flight, including our parrot!
For the parrot, the energy source is the fat stored in its body. This mass is consumed through metabolic processes that convert it into $\text{CO}_2$ and water vapor that is expelled during respiration, and as sweat and urine as the parrot flies (the parrot's "exhaust" as it were!). The energy content of body fat ($\kappa$ as defined in Eq.~$\eqref{3}$) is 9 (food) Calories per gram. One food Calorie is equal to one kilocalorie which is in turn equal to 4184 Joules in SI units, see the Wikipedia article Food energy.
The efficiency of converting stored energy in the human body into mechanical work has been estimated to be $18\%$ -- $26\%$ (see Wikipedia page Muscle). One would expect similar numbers for other warm blooded vertebrates, so that, to one significant figure, we take $\eta = 20\% = 0.2$ (a dimensionless quantity).
There seems to be a very broad range for the percent of body mass that is fat. Some migratory birds have up to $70\%$ (see Obese super athletes: fat-fueled migration in birds and bats, however the parrot is not generally considered a migratory bird. The web page Comparison of flight mileage for various wild parrot species states a migration distance of 320 km for Thick-billed Parrots for example. Hence the $70\%$ number is likely far too large. At the other extreme, ground beef is considered lean if it contains $10\%$ fat, but more generally it is closer to $20\%$. We will select a value somewhat below the median of these extremes, say $35\%$.
A typical mass for a parrot is another difficult number to ascertain, as there is a very large difference in body mass for the various members of the parrot family. For example, the web page Average Bird Weights of Common Parrot Species gives data for 52 parrot species with links to four other species, each with several entries. These vary from 10 grams for the Zebra finch to 1530 grams for the Green-winged Macaw covering a mass range of over two orders of magnitude! Upshot: there is no such thing as a "typical" parrot! We will choose the Thick-billed Parrot as we have some long distance data to compare our result to. The Wikipedia page Thick-billed parrot gives its mass range as 315-370 grams, we shall use 370 grams so that $m_{p_0} = 0.37 \, \text{kg}$, $35\%$ of which is to be considered fuel so that $m_{f_0} = 0.16 \, \text{kg}$ leaving the parrot's 'empty mass' at $m_{p_e} = 0.24 \, \text{kg}$.
We have one remaining parameter to estimate, that being the glide slope angle, $\alpha$, used to find the lift to drag ratio above. Consider the order of magnitude estimates of $\alpha = 10^0 = 1\, \text{radian} \approx 60^o$, $\alpha = 10^{-1} = 0.1\, \text{radian} \approx 6^o$ or $\alpha = 10^{-2} = 0.01\, \text{radian} \approx 0.6^o$. Clearly $60^o$ is far too steep and $0.6^o$ is much too shallow, leaving $6^o$ as the only acceptable order of magnitude choice, hence we set $\alpha=10^{-1}$ radian, a number valid for most birds of flight.
Repeating Eq.~$\eqref{8}$ above,
$$
r_m = \frac{\kappa\eta}{g\tan\alpha}\ln\left(\frac{m_{p_0}}{m_{p_e}}\right)
$$
and substituting the parrot's values from above (including unit conversion factors)
$$
r_m= \frac{\left[\left(\frac{4184\,\text{J}}{\text{gm}}\right)
\left(\frac{1000\,\text{gm}}{\text{kg}}\right)
\left(\frac{\text{kg m}^2}{\text{J s}^2}\right)
\right] \left(0.2\right)}
{\left(\frac{9.8\,\text{m}}{\text{s}^2}\right)
\left(\tan\left(0.1\right)\right)}
\ln\left(\frac{0.37\,\text{kg}}{0.24\,\text{kg}}\right)
\approx 370 \text{ km }
$$
we find the answer to the question, "How Far Can a Parrot Fly [under power] in a Single Day?" to be
$$
\boxed{r_m\approx 370\, \text{km}}
$$
a number which is in close agreement with the (limited) data available which gave an actual (vs maximum) daily migration range of 320 km.
It's interesting to note that this maximum range for powered flight can be viewed as the minimum range when gliding flight is included. Under ideal weather conditions, the actual maximum range could be extended considerably if the parrot were to capitalize on any available thermals it encountered during its flight.


text:
Do any animal have a tendon repair process that is more efficient than in humans?
Tendon injuries are notoriously slow to heal for humans, and quite often do not heal properly due to a variety of reasons. Do any animal have a tendon repair process that is more efficient than in humans? Efficient = faster + higher repair quality. If so, what property(ies) make the  tendon repair process more efficient?

I unsuccessfully searched for "tendon repair in animals" on Google and Google Scholar.

There are vertebrates that can regenerate an entire limb. Possibly there are thousands of animals that are better than humans in tendon repair. Moreover, asking an explanation for all the factors that affect tissue healing is a broad question. You should narrow down your question a bit.

@WYSIWYG Good point, let's restrict ourselves to the animals that cannot  regenerate an entire limb. Note that while there might be a fair amount of animals in that situation, our knowledge of tendons in animals is quite far from perfect, so the amount of animals known to be in that situation is most likely much more limited, if any. E.g. we only understood quite recently that frogs jump so high thanks to their tendon properties (https://news.brown.edu/articles/2011/11/frogs).


text:
Want to know about a creature which bite me

I am Sachin from MP India. Few minutes back I have gotten bite by a creature. What is its name? Is it harmful if I got bitten by it? Feeling little pain there.

Hi Sachin, welcome to Biology.SE! Please review our [help] page and our species-identification guidelines. You must include the specimen size or some approximation of it. Also, the more specific you are about your location the better -- 2 things: 1) is "MP" Madhya Pradesh? and 2) what kind of habitat did you find this in? (urban, forest, mountain, aquatic, etc.).

That is an insect, in the order Zygentoma. These are harmless, and do not bite. If you were bitten by something, it was not this?

Who is "we". I find long-winded, padded answers extremely annoying when all the person wants to know it whether a bug can hurt them. Go ahead and remove it. I answered the question.


text:
Chemical inhibition of fertilization in plants
Are there any chemical compounds that inhibit fertilization in plants after gametogenesis? Simply put, I am talking about spermicide or emergency contraception for plants.
Specifically, I am searching for a compound that will inhibit fertilization of an ovum when a pollen grain has already contacted the stigma. This compound may be effective before or after the pollen tube has formed, but ideally before zygogenesis. Although, I am also interested in compounds that prevent maturation of the zygote (basically an abortive action).
The compound is effective when applied externally to the plant (via a liquid spray, for example). Alternatively, it could be absorbed via roots or some other route.
The compound may be a small-molecule or macro-molecule.


text:
Black and orange spider, what is it?
Found in Alexandria MN, on sidewalk. Small, fast little spider.

It looks to me like one of the Amaurobiidae - the Hacklemesh weavers, often called Lace Spiders for their fluffy, cottony silk snares/shelters that they spin under rocks and logs.  It's an adult male from the big boxing glove pedipalp structures in front of the face, which is presumably why it was out in the open; it was looking for love.
As to which one it was, I'm not entirely sure - these are not a group I'm too familiar with, and I don't even know what species are found in Minnesota.  It looks a bit like a male Amaurobius ferox (an introduced European species that is spreading across the country from eastern N. America), but even lightening the photo doesn't help reveal the abdominal pattern, I'm afraid.  I'll just go with "probably Amaurobiidae" and suggest you send the photo to Bug Guide for the attantion of the pros over there:  https://bugguide.net/node/view/6/bgimage
Here's a representative male A. ferox for comparison, but note that this is a well-lighted photo so you can see the pattern on the abdomen.  Also note that there is a fair amount of individual variation in these (as in most) spiders, so some are darker, some are lighter, some have obvious patterns, some are more poorly-defined, etc.


text:
What buffer should I choose for IEX chromatography for purifying IgY
I will use ion exchange chromatography with an anion exchange column to purify chicken IgY. Prior to this I did dialysis to remove salts from previous purification steps, is it possible after this step to just change buffer system?
The pI of IgY is 5.6-7.6, and so, what buffer should I use for the chromatography? I know I want the IgY to be negative, so I would want pH in start buffer to be higher than pI?
I bought a column but it has not arrived yet. Does it come with recommendations on preferred buffer system for the chromatography or can I use any one I want? And also, what buffer should I use to elute my protein?
Do you have any recommendations?
In previous steps, prior to dialysis, I used phosphate buffered saline with pH 7.
Thanks in advance

Your column manual will probably come with buffer recommendations (these manuals are also often available online). You can also search for publications that have purified IgY by anion exchange chromatography and use their procedure as a starting point.
Some generalities to keep in mind for buffer selection:

Buffers are most effective when the desired pH is close to their pKa. A rule of thumb is to choose a buffer with a pKa within 1 unit of the desired pH.
For anion exchange, the pH should be higher than the pI of the protein so that it carries an overall negative charge and will bind to the positively charged column. Another rule of thumb is to keep the pH about 1 unit above the pI. If the pH is too low, the protein will not bind. If the pH is too high, the protein will require more salt to elute, which can cause instability/precipitation.
For anion exchange, the buffer itself should be neutral or positively charged so it does not bind to the column. This can affect binding of the target protein both by its ionic strength and localized changes in pH.
Choice of pH depends on whether your column is "strong" or "weak". The charge on the functional group of a strong ion exchanger will not appreciably change over a wide range of pH whereas the charge on a weak ion exchanger is only maintained over a relatively narrow pH range.
This may go without saying, but make sure that your protein is stable in the buffer and pH you select. You may also want to keep in mind the buffer requirements of any downstream applications and choose one that is compatible to simplify purification.

Elution is generally done with a salt gradient, though a pH gradient can also be used. In a typical setup, you would have two solutions, both with the same buffer and pH but one with high salt (let's call it B) and one with no salt (let's call it A). The sample is applied in buffer A and then a gradient from 0 to 100% buffer B is applied to the column with fractions collected periodically. The most commonly used salt for ion exchange is sodium chloride (so the counterion for anion exchange would be chloride). Since relatively high concentrations of salt are often used for elution, in general you want to avoid counterions like sulfate that have a stronger salting-out effect.

You're simply the best!


text:
What about this bat?
This happened in LaGrange GA. We heard some crawling around behind one of the faux-wood shutters on our front porch. So I eased it back and saw this:

If you can't make out the scale, the furry part was about 3 inches long. I didn't want him hanging out right there so I took the shutter off and tried to carry it to the woods but he jumped off. I videoed this:
https://photos.app.goo.gl/NsAFrcry8nJmykzQ7
He definitely had trouble flying but he didn't seem to be sick. He didn't look like a baby to me but I'm not familiar. Any idea what his problem was? He's currently either in the holly bush right next to the house or made his way to the woods in the back yard. I've heard horror storied about rabies so I avoided direct contact the best I could considering how cool this was to see one this close.

Rabid bats can't typically fly or cling upside down. (just like rabid squirrels and raccoons, for example, can't easily climb up trees). As a word of caution, you should never handle a bat you find lying on the ground because its chances of carrying rabies is much higher than one that is flying. Any oddly-behaving (or even oddly-located) bat should be assumed to be rabid simply for safety sake.

However, your bat was found clinging upside down -- a normal behavior, and one that an advanced case of rabies would make more difficult. I'm assuming the lack of flying is due to either an injury you caused to it or simply because you woke the thing up by tearing apart its house. Imagine how you'd stumble about in the middle of the night if a tornado tore off your roof and an earthquake shook you out of your second floor window!

Just an important note for those visiting this page: MOST BATS DON'T HAVE RABIES. For some more quick info: https://www.cdc.gov/rabies/bats/education/index.html

Also, in case your link eventually dies, please convert a portion of your video to a gif to post directly to SE imgur. Try www.ezgif.com to convert and crop your video to an animated gif image. Thanks

Good to know about rabid bats not typically being able to fly or hang upside down. For what it's worth, I was very gentle taking apart his house. Plus, I was there first.

 Short answer
Appears to be an evening bat (Nycticeius humeralis) or little brown bat (Myotis lucifugus).
 Long answer.
You can see a list of common bat species in Georgia through the Georgia Department of Natural Resources. (A high-res image of a visual poster can be seen here).
According to Greenhall and Frantz (1994)1, three of the species found in Georgia are among the species most found in and around buildings: big brown bat (Eptesicus fuscus), evening bat (Nycticeius humeralis), and little brown bat (Myotis lucifugus)
Your image is relatively good, but it does not provide enough detail of key structures to definitively say which species it is. (see Morgan et al. (2019)2 for a key).
If we go simply based on size, the evening bat seems to be closest to your specimen:

E. fuscus is typically 4.1-5.1 inches in length (source), which is larger than your specimen
Your specimen is larger than a typical M lucifugus (1.8-2.3 inches, source).
N. humeralis is more similarly sized (average is 3.4 inches, source).

It appears that your bat has a broad nose, which would hint toward big brown bat (Eptesicus fuscus) or an evening bat (Nycticeius humeralis).
According to GeorgiaBiodiversity.com:

The evening bat is commonly confused with the big brown bat due to its fur color and broad muzzle. However, the evening bat is much smaller and does not have a keeled calcar. The evening bat's rounded tragus distinguishes it from all other small bats except the eastern pipistrelle, which has tri-colored rather than bicolored dorsal fur. The evening bat also has just two upper incisors instead of the four typical of all myotis.

Wait, keeled calcar? Huh?

A calcar is the spur of cartilage coming off the lateral side of the ankle of bats. The image below roughly dmeonstrates the difference between keeled and not keeled.

 Left is keeled; Right is not keeled. Source: Fig 12, Morgan et al. (2019)2
Your specimen does not appear to have a keeled calcar, which would suggest further that this is more likely an evening bat versus a big brown bat.
However, the little brown bat also lacks a keeled calcar....
Though many sources do not directly compare the little brown and evening bat, Morgan et al.'s (2019) key splits these species at the same step, suggesting they have much in common. Morgan et al.'s  differentiating characteristics for these species include:

Hair on hind foot extends beyond tips of claws; tragus long and blunt; underwing lightly furred to elbow: Myotis lucifugus (Little Brown Bat).
No long hair on foot; tragus is short, blunt and curved; underwing, muzzle, and uropatagium are hairless: Nycticeius humeralis (Evening Bat)

According to Greenhall and Frantz (1994)1,

[the evening bat] bears some resemblance to the somewhat smaller little brown bat (M. lucifugus) but can be identified by its characteristic blunt tragus.

To reiterate, the "sharply-pointed" tragus (source) of M. lucifigus and the presence of long toe hairs extending beyond the length of the toe claws (source) would both definitively point toward the little brown bat vs the evening bat. However, neither characteristics is really distinguishable in your photograph.
As such, I don't feel fully confident to rule one out over the other.
It's 3 am though, so perhaps I should stare at your image more in the morning after some rest...I'll update further if I notice anything definitive.

 1. Greenhall, A.M. and Frantz, S.C., 1994. Bats (Myotis lucifugus). The Handbook: Prevention and Control of Wildlife Damage, p.46.
 2. Morgan, C.N., Ammerman, L.K., Demere, K.D., Doty, J.B., Nakazawa, Y.J. and Mauldin, M.R., 2019. Field identification key and guide for bats of the United States of America. Occasional papers (Texas Tech University. Museum), 360.


text:
is this a brown recluse spider?
What kind of spider is this? SE Michigan, light brown color, second picture less focused but w tape measure for scale. Thank you!

Here's a good image of a brown recluse: https://upload.wikimedia.org/wikipedia/commons/c/cc/Brown_Recluse.jpg. Notice the characteristic violin shape on its head.

No, this is not a Brown Recluse.  There are several reasons for saying that, among them the fact that it's outside; it's hanging on a screen, and it doesn't look at all like a Brown Recluse - (Recluses don't have a rectangular cephalothorax "head end", and they have a bulbous abdomen, not that pointy-ended one this spider has).
As for what it is, there are some good clues - first that rectangular-looking cephalothporax.  That's pretty unusual in spiders, although it's not actually rectangular; it's just the central dark pattern is very blocky.  Then, look at that color - kind of a creamy light mahogany rather than a real brown, and no darker/lighter patterns that the bigger wandering spiders that look like this would have.  Finally, look how it's holding its legs - both the front pairs are close together.  That's something you tend to see in two sorts of spiders - the big Argiope orbweavers, and the big Fishing Spiders and their relatives.  Argiopes have a different body shape, pattern and color than this, and it would be a little unusual to find one this size hanging around not in a web.  Fishing Spiders are generally dark-colored, and with more patterning than this, but there is a close relative that fits this image:  the Nursery-web Spider, Pisaurina mira.  Here's the Bug Guide page, and a representative photo:
https://bugguide.net/node/view/2919

John, excellent descriptive answer. I always appreciate how knowledgeable you are regarding spiders. Is this based on experience / collected knowledge, or do you use a key/guide? If the latter, which resource do you use?

Yes to echo @theforestecologist these are the sorts of species ID answers that I really appreciate: those giving a description of the attributes that led an expert to their conclusion. Well done, thanks for your work.

Thanks - unfortunately, up until recently, there really weren't any particularly good field guides to spiders.  There was the Zim Golden Guide, which had some common species, and fairly recently there was the Audubon photography-based Insects and Spiders, which had a few species as well.  I learned using the very good Kaston lab guide, and collecting spiders enough to learn the various groups by eye.  It's not too hard; just takes time and practice (and an interest in learning about spiders, of course).  Nowadays there are several good websites, of which Bug Guide is the best.

If I was learning now, I think it would be a bit easier because Richard Bradley's really excellent book covers many of the more common species, and does it very well.  Still, there really is no substitute for field observation, so you can recognize the patterns of stance, shape/colors and behavior.  You may not know the specific spider, but you generally have a guidepost to help you narrow it down.  It's like with birds and trees and flowers, but without the useful pocket guides..


text:
Is that a sundew?

I have bought the seeds for a sundew/drosera (growbro.nl) but I have pretty serious doubt if that is really the plant I wanted :-)
If not, what kind of plant is that I have grown?

This is not a sundew. A simple Google search can confirm that.

Thanks. I still hoped that it is maybe just a transition phase and it will look as the actual sundew.

That looks a bit like a member of the genus Impatiens some members of which are invasive.
Some images can be seen here.
Flower pictures would be helpful for identification ...


text:
How can parentage test be accurately done even though crossing over occurs?
As crossing over occurs when gametes are secreted, so when a zygote is formed after fertilization, the base pairs of DNA in the child should be different from that of the parents. So when gel electrophoresis occurs, the position of DNA fragments of the child shouldn't be the same as half of their father and mother. But why is this statement wrong? sorry for bad English.

Crossing over is an event that occurs during meiosis, which produces the gametes. This crossing over occurs between 2 homologous chromosomes, which are both from the parent. Hence, even though crossing over occurs, the recombinant chromosome that is passed down to the child will contain an allele that matches with the allele on one of the parent's chromosomes. Within the allele, the base pair sequence would not change.

So it means that the allele extracted from the child should be the same as the parents to attain the same base pair sequence? i.e. tandem repeat? Thank you very much

Yes, the same allele should be targeted in the child as in the parent. This would ensure that the size of the DNA fragments obtained are the same, so the position of the DNA bands on the gel would also be the same.


text:
Can mammals and/or birds see / detect infra-red light?
Wondering if there is any evidence that mammals or birds eyes can detect light emitted in the infra-red?  The reason I'm asking relates to the use of nest cameras to detect predators, using infra red LED light to take pictures at night.  New technology allows a picture to be taken every 3 seconds, throughout the night.   Clearly if these can be seen - then a mammal, or nocturnal bird could quickly learn to look for the flashes of light and find a tasty source of food...

they can detect it sure, just like we can feel heat from sunlight on our skin.

Pit vipers do but not using their eyes and they are not mammals or birds.

https://physics.stackexchange.com/questions/147746/why-human-and-most-of-vertebrates-cannot-see-near-infrared-light-720nm-1500nm

Infrared is a fairly large part of the electromagnetic spectrum, so to get an answer best suited to your specific case, you should specify the wavelength of your LED. There is at least one study showing that ferrets (not sure if it's the best predator to worry about for what I assume is a suspended bird's nest) can see up to 920nm.
So to answer your question, yes, at least some can, but the further into the spectrum you go, the fewer there will be.
I am much less certain, however, that this would attract danger. Nocturnal predators in biomes inhabited by humans generally evolve to avoid rather than seek out artificial light sources.

Thank you so much TheChymera.  The camera LED's are in the 950-970 nm range - so looks very likely they will be out of range of mammals... and hopefully birds too, although I'm not aware of any evidence here - just seems likely.


text:
Why are mammals the only animals with pinnae / outer ears?
Yes, I know owls have feathery "ear tufts", but these are less suited for hearing and more for display.
And I find it hard to believe that animals like dinosaurs or other cursorial archosaurs would not rely on sound as much as a mammal would. It's just too useful of a sense.
One potential clue is the fact that most non-mammal tetrapods appear to use electrical tuning to discern different sounds, whereas mammals use the hair cells of their longer cochlea to mechanically discriminate sound. I feel like this is related but not completely connected to why a fleshy outer ear structure that can collect and focus in on the direction of a sound.
Why did the pinnae evolve in mammals and why are they the only ones with such a structure?

If an organism does not have outer ear, it does not mean it does not rely on sounds. Birds heavily rely on sounds for so many aspect of their life. Owl is a great example,

Which isn't the question. The whole idea of the pinnae is that they aid in the collection and focusing of sound, yet other animals seem to be able to do this relatively well so there must be some reason they don't have pinnae.

I understood (maybe misunderstood) the sentence I find it hard to believe that animals like dinosaurs or other cursorial archosaurs would not rely on sound as much as a mammal would as assuming that absence of pinnea means poor use of the sense of hearing.

Indeed. It was more of a rhetorical doubt.

Do you really think there can be an objective answer to a question of the form “why did this NOT evolve in any other animals? All you end up with is circular arguments of the type that are the very antithesis of science. The one answer you have so far just describes the thing and says how wonderful it is.

@David The question is literally "why did this evolve in only one group of animals", and I just got such an objective answer. It's always puzzled me why StackExchange users try to belittle the OP into thinking their question is stupid/too broad/impossible to answer while it clearly isn't that insurmountable.

I think it is worth noting that not all mammals have pinnae (the external component of the ear) – i.e. Australian monotremes and the marsupial mole. Also, props to T-Rex for calling out the online bullying, which is totally unnecessary.

Ear pinnae in Katydid insects to detect bat ultrasounds: https://doi.org/10.7554/eLife.77628

Short answer Mammalian hearing is unique and amazing.
The mammalian ear is unique and highly sensitive with a built in amplification system that means even minute changes in sound can be detected. The bony amplification is also the reason the mammalian (or at least therian) cochlea is huge, every incremental increase yielded markedly more information, it has to get quite large before you hit the point of diminshing returns. This means mammals can get a lot out of even small investments into improving hearing. The vast majority of other groups just would not get any benefit from an external ear. their ears are not sensitive enough to gain anything the faint echoes external ears collect. The one group that would get some benefit (owls), has something functionally similar to an external ear.

The mammalian ear evolved from the repurposing of vestigial jaw bones no other group had (or more correctly they did not become vestigial in other groups). Mammals are the only group with a single bone in the lower jaw. it is a fascinating story and well worth a look. It kinda makes up for how awful mammalian eyes are.

A Lizard would need ears of 8cm to focus it's upper hearing range.
Lizards and birds can hear as high as 4kHz to 10 kHz, which corresponds to an energy wavelength of 8cm to 3cm, so a frog would need ears of about 8cm to collect and focus the sound, and a bird would need ears of about 3cm. Bird calls are also mostly limited to about 8khz, about 1 octave higher than note 88 on a piano.
Also, the distance in between the two ears of i.e. a bird is less than the wavelength of the sound that they detect, so they have less sense of which direction sounds come from.
Cats and mice can hear sound waves of about 0.5cm, so their ears can augment and focus the sound efficienty and can also shield the ears so they just hear one side each.
Soft materials absorb sound, that's why audio speakers use carbon fiber and other rigid diaphragms to transmit high frequencies, and that's why toast has higher frequencies than bread, so mammals had to use the stiffness of articulated bones to pick up high frequencies of sound. It's a complex adaptation step, a bit like the evolution of the eye.
Here is a vid about mammal ears the wiki.
Early mammals were nocturnal, it may be a contributing factor.

The argument on body size / sound wavelength doesn't stand much with large dinosaures, does it?

Yes, it's more likely that a dinosaur could evolve giant ears to amplify and locate sound, especially if it's a nocturnal avian dinosaur. it's the high-frequency limit of a vertebrate's inner ear relative to it's size that influences if it would benefit from ears. Birds and lizards would have evolved ears if they didn't need giant ears relative to body size because their inner earbones are intrinsically limited to big wavelengths. Say a dinosaur has an upper hearing range for 5cm wavelengths, and it had 5cm ears.


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What bug is this

Found in Mojave county Az. It was in my home. I have a cat.  Real small about 1/8 inch

Three questions: 1) Did/does it have relatively long antennae not visible in picture? 2) Did you only find one? 3) Can you provide a top-down photo?

I can't tell if it has an antenna. I have found in past. Sorry this is the only pic

If viewed from above, does this insect appear to be very narrow (somewhat flat) from side to side, or does it look about as thick as a "normal" bug?


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How does Line Integrate work on a laser scanning confocal microscope?
Most microscope software provides options for line average or line integrate as a function that helps the signal to noise ratio when taking an image. The math behind line average seems straight forward, but not so much for line integrate.
Line average takes X number of scans per pixel and averages the scans into a final pixel intensity. The same principal of multiple scans for a single pixel is taken for line integrate, but the math involved in the integration of the intensity is not clear to me. I assume it involves summing pixel intensity and operating on that somehow, but it simultaneously is able to reduce noise in the system so I am not sure what else it is doing.

Most microscope software provides options for line average or line integrate as a function that helps the signal to noise ratio when taking an image.

Averaging sums the lines and then divides by the average number. Integration sums the lines without dividing.  They're functionally the same thing just with different scales.

I assume it involves summing pixel intensity and operating on that somehow, but it simultaneously is able to reduce noise in the system so I am not sure what else it is doing.

In terms of shot noise, both have an equal reduction.  If you are averaging over extremely dim signals at low gain (particularly those averaging less than 1 DN per pixel), integration can save you signal from being rounded down to zero.


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Schizocoely and Enterocoely
In terms of phyla, mollusca, annelida and arthropoda are schizocoelic, whereas echinodermata and chordata are enterocoelic.
I know that their difference lies in the formation of the coelom but how exactly is enterocoely more advanced than schizocoely?

Neither is "more advanced" than the other, they are separately evolved mechanisms to form a gut.
You may be misled by a human-centric view that treats humans and animals more humanlike as more advanced or "more evolved" than other animals but this is not true: all life has been evolving for the same length of time.


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Identify round, green, flying insect with spikes in South Carolina (USA)
The tables have turned -- I need some help IDing an insect:
I've been unable to identify an insect that I came across about 6 years ago in South Carolina (USA).
We were doing a vegetation survey in a northern South Carolina forest when I felt a pinch (or bite) feeling on my hand. When I looked down a seemingly nearly round insect was at the site of the pain but flew away shortly after.
I have no photo of the insect, unfortunately, but I can best describe it as being light green, round (0.5-0.75 cm diameter) and shaped like a deep (i.e., slightly recessed) dinner plate with a ring of soft spikes around the perimeter of the slightly raised edges of its round body. I unfortunately have no recollection of the head or wings.
Here is a rough sketch of what I remember:

The spikes were very reminiscent of the backside of some adult scale insects (such as here) [seen below].

Given it's similarity to some scale insects, I've always assumed it was some species in the Coccoideae superfamily, but I have never been able to find a matching species.
Anyone have any ideas?

The only green spikey insect I've found to date is Spissistilus


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How does X chromosome monosomy occur
I want to understand how Turner syndrome - monosomy X - occurs at the molecular level. The NIH mentions that there are cases of both complete monosomy and of mosaicism.
I’m particularly interested in the monosomy case, as this really confuses me. How does a fertilized egg end up with only one sex chromosome (an X, in this case)? Is an empty egg fertilized by an X-bearing sperm? Is an X-bearing egg fertilized by an empty sperm?
The case of the mosaicism is easier to imagine - say through X chromosome nondisjunction at a very early point in some cells of the embryo. NB: unsure this is actually how mosaic monosomy X happens.
I haven't found a source that doesn't begin from the point at which monosomy has already occurred.
How do things get to that point? Where and how is a sex chromosome lost, such that a human can develop with only the one?
Thanks so much for any pointers!

Most often, it seems that Turner syndrome is due to fertilization by a sperm cell lacking a sex chromosome. I wouldn't describe such a cell as "empty": it still has the other 22 chromosomes, but in meiosis the sex chromosomes failed to segregate appropriately.
Monroy et al 2002 note that of 10 people with complete monosomy X, 9 had their single chromosome from the mother.
Monroy, N., López, M., Cervantes, A., García‐Cruz, D., Zafra, G., Canún, S., ... & Kofman‐Alfaro, S. (2002). Microsatellite analysis in Turner syndrome: parental origin of X chromosomes and possible mechanism of formation of abnormal chromosomes. American journal of medical genetics, 107(3), 181-189.

Thank you! I hadn't found that reference earlier. Definitely helps me to understand it better.


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How does the structure of tendons change as they become stronger?
I understand the basic structure of tendons, but I wonder how a tendon becomes stronger via exercise. Do the collagen fibers become more aligned/numerous/dense/etc.? Is the tendon expected to become thicker as it gets stronger? Does the cellular content of the tendons somehow change (e.g., more tenocytes, or higher quality tenocytes)? What other factors have a role in tendon strengthening?


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Why are there two abrupt changes in the genome sequencing price curve?
In the price curve of the genome, from NIH:

NIH explained the abrupt drop at 2008 thusly:

beginning in January 2008... the sequencing centers transitioned from Sanger-based (dideoxy chain termination sequencing) to 'second generation' (or 'next-generation') DNA sequencing technologies.

The NIH did not give any details as to why there was a similarly precipitous drop in 2015, or why there was such a saddening (for me!) plateau after that. Please explain them to me?

This graph from the Broad's Opinionome blog (ugh) is somewhat more annotated:

As noted elsewhere, the precipitous drop in 2007 is almost certainly due to maturing next-gen sequencing (NGS), in particular Illumina.  Illumina acquired Solexa in 2007, which offered gigabase-level sequencing ability.  In 2014, President of Illumina Francis de Souza essentially said as much:

During the EmTech conference, De Souza said Illumina’s success was due to a “hard pivot” the company made in 2006, when it got into the DNA sequencing business by acquiring Solexa, a U.K. startup, and bet its fortunes “on a technology with no sales, that no one knew if it would work.”

Essentially, by 2007/2008 you had stellar technology+company hard-selling it = adoption
I'm less certain about the less-dramatic drop in 2014/2015, but I agree with Franck that it's likely largely be due to the introduction of the Illumina HiSeq X Ten in early 2014.  You can read some corporate spam, but it was indeed a big deal.  There were other technologies that probably played a role (new PacBio system released in 2013, etc.) but Illumina was and is top-dog.
None of this takes into consideration increased interest in such research, or the faster computers, larger SSDs, and expansion/normalization of multi-core systems that makes working with such data easier.

The "opinionome" is the oddest use of "-ome" I've seen so far lol

@MaudPieTheRocktorate This is likely intentionally tongue-in-cheek, but a friend and I used to keep a list of wild -omics words in published papers, and... yeah, there are some categorically absurd ones.

Would you give a few examples? For the lolz of posterity.

Some I consider begrudgingly fine — injectisome, translatome, inflammasome — while others are bad and feel like they're trying to make "fetch" happen — promoterome, ligandome, connectome — and others are just beyond — HAR-ome, imagenomics, screenome.

The graph is in contradiction with the data in the Excel spreadsheet the same webpage provides (https://www.genome.gov/sites/default/files/media/files/2019-06/Sequencing_Cost_Data_Table_Feb2019.xls (mirror)), which I plotted below:

Update on 2019-11-17: I contacted wettersk@mail.nih.gov and the graph on https://www.genome.gov/about-genomics/fact-sheets/Sequencing-Human-Genome-cost is now fixed:

https://en.wikipedia.org/w/index.php?title=\$1,000_genome&oldid=902062326#Commercial_efforts to some of the dates on the reaching the 1000 USD/genome goal, and doesn't indicate any plateau:

In January 2014, Illumina launched its HiSeq X Ten Sequencer, claiming to have produced the first \$1,000 genome at 30× coverage. Some researchers hailed the HiSeq X Ten's release as a milestone – Michael Schatz of Cold Spring Harbor Laboratory said that "it is a major human accomplishment on par with the development of the telescope or the microprocessor". However, critics pointed out that the \$10 million upfront investment required to purchase the system would deter customers. Furthermore, the \$1,000 genome cost calculation left out overheads, such as the cost of powering the machine.[25] In September 2015, Veritas Genetics (co-founded by George Church) announced \$1,000 full-genome sequencing including interpretation for participants in the Personal Genome Project.[26]
In April 2017, the newly formed European company Dante Labs started offering the WGS for \$900.[27][28] In 2017, Beijing Genomics Institute began offering WGS for \$600.[29] In July 2018, on Amazon Prime Day, Dante Labs offered it for \$349.[30] In November 2018, around the time of Black Friday, Dante Labs offered WGS for the first time less than \$200,[31][32] and Veritas Genetics for two days for the same price of \$199 offered WGS limited to a thousand customers.[33] In March of the same year, geneticist Matthew Hurles of Wellcome Sanger Institute noted that the private companies, including Illumina,[34] are currently competing to reach a new target for WGS of only \$100.[35]

Page summarizing current prices: http://arep.med.harvard.edu/gmc/genome_services.html (mirror).
Update (2019-07-03) https://www.cnbc.com/2019/07/01/for-600-veritas-genetics-sequences-6point4-billion-letters-of-your-dna.html (mirror):

Veritas is lowering the cost of a full genome sequence from \$999 to \$599 and believes within two years it will be pricing in the \$100–\$200 range.

Another price progression plot from https://youtu.be/jH87sfVD36M?t=554 ("George Church - Cognition Genes. Aging Reversal. Lab-built Brain Components"):

Illumina launched HiSeq 2000 in early 2010 after purchasing it from Solexa in 2007  http://dx.doi.org/10.1155/2012/251364

By "contradiction" do you mean the mistake in the y-axis labeling?

@tyersome yes that seems to be the issue

I'm not 100% sure, but I think Illumina launched their HiSeq machine around that time, massively increasing the sequencing output in one run. That dip might be related to that.


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Heritable immunity and smallpox vaccination
As I understand it, lack of heritable immunity caused smallpox to wipe out certain communities of native Americans. If vaccination conveys heritable immunity to a population, shouldn’t this make vaccines unnecessary after the first generation?

Genocide is not a verb.  Nor does the death of a large number of people in a plague constitute genocide, whether it was the introduction of European diseases to the Americas, or the introduction of Asian or African diseases to Europe, e.g. the Black Death, the Plague of Justinian, &c.  You might also note that smallpox was endemic or epidemic in Europe and the Near East for centuries prior to the development of vaccination, regularly killing significant numbers of people.

Yersinia pestis was not a new European disease in 1300...

I have edited your question for logic (inserted “lack of”) and to make it conform to scientific and non-confrontational site style. As a new user to this list I would encourage you to take the Tour and read about asking good questions.

Guys, you are discussing with an anti-vaccine troll, as the original not edited question clearly shows.

@Chris I am not discussing with him, although jasmesqf is. I edited his question so that we can post a clear answer clarifying the confusion in the use of the term immunity and making the point that the immune response invoked by vaccines is not heritable. It is important, however, not to get side-tracked into answering questions about when bubonic plague appeared in Europe and to provide basic references in answers. I intend to reply  myself, to some extent duplicating what Bryan has said, but focusing on what I have just said, not accepting undocumented interpretations of history.

@Chris It may have been convenient to close this as a duplicate, but in my opinion it was wrong to do so. The question this is a supposed duplicate of is different and is a historical question which can only be answered in a speculative manner. It is extremely badly phrased and should be closed, rather than this question as now amended which asks a precise scientific question which can be answered clearly and unequivocally without any reference to historical events and for which an answer could be used as a resource.

@Chris: You are less charitable than I am.  I'm assuming s/he is just ignorant, or perhaps deluded by anti-vaccination propaganda, and so possibly could be educated.

@jamesqf I was just saying that discussion might be pointless. You are if course fine to do this (the question now is ok I think), but I will have an eye on this.

Vaccines are pointless?

No.
The heritable immunity you are describing is due to selective pressures on populations where individuals with certain alleles have a survival advantage in the face of particular pathogens. If a population is exposed to deadly diseases like smallpox and there are some individuals in the population who are more resistant, those individuals are more likely to survive to reproduce so future generations will have more resistant individuals. You could think of this as immune system "hardware."
Vaccines trigger the immune system's ability to recognize past infective agents and therefore mount a rapid specific antibody response when exposed to that pathogen again. You could think of this as immune system "software." This software that is aquired during the lifetime is not present in the genome of germ line cells and is not transmitted to offspring.

Is there any scientific evidence or specific mechanism(s) for what you a re saying

@user52352 You can read about the adaptive immune system starting with Wikipedia https://en.wikipedia.org/wiki/Adaptive_immune_system or any biology textbook. To learn about evolution and heredity you can start with https://evolution.berkeley.edu/evolibrary/home.php

Those don't seem to mention the genocide if the native Americans, or your hardware distinction whatever is meant by that


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How can I change my buffer system for protein purification?
I have a protein that I purified in PBS buffer, pH 7. I will do dialysis to remove salt and will then further purify the protein with ion exchange chromatography.
I will need to use another buffer (Tris-HCl) with pH 8 in the chromatography, and so my question is: Can I change the buffer system for my protein in the dialysis step? Or would you recommend me to use the Tris-HCl buffer from the very start and then just adjust the pH for the chromatography?
Thanks in advance!

Assuming that your protein can handle being in the new buffer, you have multiple options.
Dialysis will work although you might want to consider using a centrifuge spin filter with a suitable MW cutoff to gradually switch buffer and concentrate the sample. Be aware that some of your protein will stick to the filter, giving a loss of sample.
Alternatively you can perform size exclusion chromatography to switch into the new buffer, but you better be sure that the sample will remain stable or you may clog the column. If you can perform affinity chromatography, you can also opt to change buffer in this step.
You can of course try to start with a Tris based buffer and simply adjust pH by dialysis in a tris buffer with the desired pH. Just make sure that the dialysis volume is large enough to counteract the buffer in the sample.
Instead of using PBS you can also try with TBS (Tris-buffered saline), see wiki for details. https://en.wikipedia.org/wiki/Tris-buffered_saline

There are a number of ways to address this, and the other answers are certainly correct. Another strategy, especially if you already have the sample in PBS, is just to dilute it in the low salt ion exchange buffer. This works because you don’t need to completely remove the phosphate or salt, just get it low enough so that it doesn’t interfere with binding to the column. This method also has the advantage of minimizing the exposure of your protein to low salt, which can destabilize it, and is often used for ion exchange chromatography.
As an aside, if you’ve never done IEC with this protein before, you may want to do a trial run first with a small aliquot of your sample so you can make sure the conditions you’ve decided upon are suitable.

Good point, dilution of the sample might be the easiest way forward, if feasible in regards of sample volume and flowrates.

Two accepted methods of 'desalting' a protein and/or changing the buffer are dialysis and gel-filtration. Dialysis is time-consuming, and gel-filtration usually requires a concentrated sample (It is difficult to gel-filter a 250 ml sample unless a very large column is available, for example, but dialysis of such a volume is relatively easy).
You do not say whether you are using cation- or anion-exchange chromatography, but note that the charge on the buffering species is positive with Tris, but negative for phosphate, and it is usually desirable that the charge  is the same as that of the ion-exchange column, as you do not want the buffering species to be exchanging and possibly exposing your protein to 'local' extremes of pH, especially if your protein is sensitive to pH changes: use a positively charged buffer for anion-exchangers such as DEAE-cellulose, but a negatively-charged buffer for cation-exchangers such as CM-cellulose.  (This is the 'strategy' adopted in Chromatofocussing, and I'll bet that is why the protocol requires a change in buffer as well as pH).
Note also that a protein that binds to an anion-exhanger at pH 8 may not bind at pH 7: in Chromatofocussing on an anion-exchange column, for example, we lower the pH to elute the protein.
Ref: Protein Purification. Theory and Practice, R.K. Scopes

Impossible to answer this in detail without knowing why you started with PBS, but simpler is better so if you can start with a buffer that is compatible with the ion exchange step then I would try that.
Dialysis is a reasonable way of changing buffers, but do you know whether your protein is soluble in Tris at pH 8 without salt?
If you have a relatively large sample you might consider doing a test dialysis using a small fraction using something like this kit.


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Why is wound contraction very slow?
I am working on mathematical model for healing of dermal wounds. For anyone who's a bit familiar with Physics and Math, for the model I use the Cauchy Momentum Equation as a basis, and from there I use already established literature to expand to a so-called morphoelastic model.
From a physical perspective, if a force is exerted, you would expect a material to start moving, upon which stresses arise, until a new balance is found. This all usually happens on a timescale of second. Now when wound healing is regarded, the contraction force is exerted by fibroblasts. I have read that wound contraction happens at a speed of up to 0.75/mm per day. On the one hand this is impressive, yet on the other hand it is very slow when viewed from the mechanical perspective.
So my question is: Is there a biological effect or phenomenon that slows down? Could it be that the migration speed of fibroblasts is the bottle neck? Or maybe skin is in some way tethered to underlying tissue? I know very little about biology, so any help would be appreciated!
Thanks in advance

Is it really that slow? What are you comparing it to? If you're comparing it to simple muscle contraction, you should note that muscle movement is transient and returns to its original shape when the stimulus/energy input ceases. When a wound is healing, it wants to change its shape permanently so it's more like tissue growth. (1/2)

If you compare it with growth of maize root tips, which grow at only 2.4 mm/day or dendritic spine growth, which is only 0.13-0.17 mm/day it doesn't seem that bad. (2/2)

As far as my biological knowledge goes (which is not very far), wound contraction happens due to stresses induced by ((proto-)myo-)fibroblasts. Before, during, and after wound contraction, collagen fibres are secreted in order to replace the injured skin. The new arrangement of the collagen is reflected by the mechanical properties of the tissue.
If wound contraction was to be attributed to a tissue growth-like process, the rate at which it happened would completely make sense to me. But from what I have understood, wound contraction is a mechanical process.

Your comment actually cuts right into the heart of morphoelasticity theory, where deformations are decomposed into an elastic (transient) and a plastic (growth) component

Short Answer : You can not pinpoint any single step for this delay. It is a combination of multiple processes.
Long Answer : I think there are multiple factors that can contribute to this. Dermal Wound healing is a multi-step and complex process typically includes inflammation, new tissue formation and remodeling (Gurtner et al 2008). Each of these stages involved very complex signaling pathways of various components. In addition, there are multiple types of fibroblast cells involved in this process. You are most likely talking about Myofibroblasts who bring the edges of a wound together. However, this itself is a very complex process involving interaction with the proliferation and migration of both mesenchymal and epithelial cells. This is further tightly controlled by Keratinocyte-fibroblast interactions (Werner et al 2007).
So what can you do? : The the physical analogy, which you are trying to implement here, has to apply within some assumptions. You can declare some fitting parameter(s) which can contribute to all the process and validate it according to good experimental data, probably with some kind of mutant data where the wound healing process is slowed down or accelerated. While deciding your assumptions, use as fewer assumptions as possible else you will end up creating Spherical Cow.


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How can I get the yield of my purified immunoglobulins?
In order to get the yield of IgY through a set of purification steps, what method can I use?
Thanks in advice!

Do you know the antigen of the Ig and can you make it and use it for assays?

Someone asked a similar question recently.

You can use western blotting with a anti IgY secondary antibody conjungated to  a HRP (or other reporter), this method will primarily help with troubleshooting your purification and locating IgY in the different fractions and flowthroughs.
If you want to quantify, consider using an ELISA kit. Here is one such kit (https://www.antibodies-online.com/kit/1563240/IgY+ELISA+Kit/)


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What differentiates neurons in different parts of the brain?
For example: what makes a neuron in the hippocampus of the brain different from a neuron in, say, the amygdala, or the frontal lobe, or anywhere else in the brain? Do neurons in different parts of the brain have different structures, or are they differentiated solely by location?
By "different structure", I mean things like receptors that other neurons don't have and things like that.

There are differences in receptor expression and morphology, but it would be beyond the scope of an answer in this site's format to enumerate. The major differentiating factor is most likely the source of their inputs.

They express different genes as pointed out by @vkehayas. Is your question about why there is a difference or how the difference came to be?

During development of the brain neurons undergo several steps of differentiation. They transition from neuronal progenitors to mature neurons, resulting in different types of neurons, characterized most prominently by their primary neurotransmitter. During the differentiation, different genes are expressed, which in research is used to label specific cell types (to e.g. observe their distribution in the brain). Since timing is important in development and neurons migrate to their side of action, later born neurons often display different features than earlier ones. The final differentiation is also dependent on the environment, meaning surrounding cells can influence the outcome.
Not just neurotransmitters, also other surface molecules, types of synapses formed, morphology and many other genetic differences influence neuron function and their diversity. Each brain area has many different neuronal cell types, some are similar between brain areas, while others might be very specific to one area. As an example, there is a microRNA, expressed in only 6 neurons of the nematode worm C. elegans, that is essential for their specific function to sense CO2 by repressing other genes (publication).
Taking the example of your question, here is a paper on the diversity of GABAergic neurons in the amygdala (there are several different types of neurons having the same neurotransmitter but expressing otherwise specific markers, which results in different specific functions in the circuits). The author compares them to GABAergic neurons in the cortex (including hippocampus), where a similar function might be taken over by a different cell type (expression profiles are distinct due to different lineages and environments and can be labeled by different markers).


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Can someone identify this plant I saw in NYC (might not be native idk)
I've never seen a plant with these type of leaves before and was wondering if anyone recognized/can figure out the species.

Okay so simple solution I saw the owner of the plant out and just asked what it was. She said it was a Konnyaku Potato (Amorphophallus konjac 'Nightstick'). You can see the branching shoot at the bottom, similar colors, and similar leaves.

That looks like it is probably a single leaf coming up from a tuber.
That fact combined with the mottled pattern on the petiole (leaf stalk) and the shape and branching pattern of the leaflets makes me guess it was something in the genus Amorphophallus.
Example image:
Other images for the "voodoo lily".

please provide some evidence for why you think this is the case as well as a picture if you can find one in the public domain to share. I think you're correct, but your answer is not so great if your links die. We typically want the answers to provide more stand-alone evidence than yurs currently does, especially for [tag:species-identification] questions (in which many people provide incorrect IDs). Please [edit] to add this additional detail. thanks!

@forestecologist: Finally figured out how to insert an image — is this better?

Better, yes, But if you could provide a bit more detail (e.g.,what about the petiole is significant?, etc.) and a source supporting claims that X about the petiole (or mottled leaves, etc.) are in fact indicative of this group, your answer would be better still. Adding these types of details & references does 3 things: 1) allows you to double check yourself (especially if you haven't seen formal sources yourself), 2) provides a reader greater confidence  you're right, and 3) enables readers to easily find a (hopefully) good gateway to learning more. In other words, The extra work pays off

Thanks for the help, the actual plant was in fact of the amorphophallus genus so props on that. I'm sure we could've figured it out with some research into the genus you provided had a more direct opportunity for answers not presented itself.


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What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?
The 2018 study {1} mentions that:

The healing process
  of injured tendons includes tenocyte migration which occurs
  from intact regions of tendon into the wound site.

What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?

References:

{1} Dursun, Gözde, Mersedeh Tohidnezhad, Bernd Markert, and Marcus Stoffel. "Effects of uniaxial stretching on tenocyte migration behaviour." Current Directions in Biomedical Engineering 4, no. 1 (2018): 313-317. https://doi.org/10.1515/cdbme-2018-0076