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What species of worm is this? Found in underwear on Ecuador coast

My wife found this worm in her underwear this morning when she woke up.  It wasnt attached to her or anything. About 4-5 inches long. Redish in color and slightly see through, meaning you could sort of see its organs.
We are in Puerto Lopez Ecuador.

Do you think it's possible to be a parasitic worm? if yes it could be an ascaris lumbricoides and in that case I would recommend your wife to go to a doctor because those worms can lead to bad symptoms.

Anyway whatever is the type of worm, I would consult a doctor in any case a parasit goes out of my body.

Oh for sure. We all got on parasite meds immediately.  Definitely a parasite. Was just curious what type :)

See my first comment, the worm seems to be an ascaris lumbricoides but  I am not specialist. It would be better if a specialist in parasitology can confirm or infirm this.


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Where to find data on different crops
Hello I'm not sure if this is the proper place for this question. If not, I am happy to move it.
I'm trying to find a source of data on different crops, is there some governmental database that houses this kind of data? After looking for a couple hours on google and reading a few different articles, I have not really found what I was looking for.
For example, consider the crops maize, wheat, sorghum and sugarcane. I could be looking at the different kinds of carbohydrates an their proportions in these crops, or I could be wanting to know the amount of water needed to produce some yield, what kind of soil each crop likes as well as how different hybrids and mutants have different needs or qualities.

Did you try a google search? I got these results, hope they are useful:
http://www.fao.org/land-water/databases-and-software/crop-information/en/
https://world-crops.com/home/
http://www.ecpgr.cgiar.org/resources/germplasm-databases/eccdb-list/

source: Stack Exchange

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

sort: votes


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Where to look up animal facts concisely
Googling leads to results such as this:

DIET
  Eagles primarily eat fish, carrion, smaller birds and rodents. Eagles are also known to prey on large birds and large fish.
POPULATION
  Bald eagle numbers in the U.S. were estimated to be between 300,000-500,000 in the 1700s. Numbers were once as low as 500 nesting pairs in the lower 48 states. Bald eagle numbers have rebounded since and now the lower 48 states boast over 5,000 nesting pairs. There are a total of about 70,000 bald eagles in the whole of North America (Including Alaska and Canada).
RANGE
  Bald eagles live near bodies of water in Canada and Alaska, and in scattered locations all throughout the lower 48 states and Mexico.

I would like to find something like this but with more detail, perhaps scholarly papers or such like that, like you might find on a synopsis/summary article for a specific protein. Wondering if anything like this exists.
Examples of "facts" I would like to look up:

food sources
habitat
range
color
sound
population size
lifespan range

Stuff you see like this has few if any citations where they get the info from.

I'd write a program that can query google for complex search terms and return the related numbers, colors, phrases and paragraphs for all 10,000 most common animal species. Then simply press enter and the program could add about 100 species to the database every hour, hammering google.

@com.prehensible — Gosh! Sounds really easy. You do lot of this sort of thing?

It's called parsing. It would take literally a week to have a draft version going. I'm not very good at it, I run unity3D which does webURL queries and any code you want from it, it returns text and you just have to use string commands to search, concatenate, divide substrings. I did something like that 4-5 years ago, which builds animated 3D phylogeny trees using google image search.

@com.prehensible — you need to include the @ handle to alert anyone other than the poster to a comment. This is obviously not the place to discuss computational methods, but parsing free text successfully is a complex task, which I would be surprised to see performed with a gaming engine. And remember that Wikipedia entries are compiled by humans with at least some expertise. Who is going to tell whether pressing “enter” produces garbage or not?

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


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Replacing, instead of repairing, DNA
I've been doing some light reading on DNA damage theory of aging. One of the main ideas from that theory that I got is that the accumulation of damage in our DNA is one of the biggest causes of why we age, which is quite intuitive for a non-biology major like me. Furthermore, there has been research on DNA damage repair pathways and ways on how nanotech can help repair DNA. The technicalities are beyond me. My question is

If accurate DNA repair is such a difficult mechanism to sustain over a
  lifespan, then why not catabolize DNA and replace it with a new one?

It seems very feasible to synthesize human DNA (please inform my ignorance, if I'm wrong. lol.) and it looks very promising after reading this: https://www.wired.com/story/live-forever-synthetic-human-genome/.
EDIT: It was pointed out to me in the comments that my question is too broad, please do tell me how to make it more specific, if you agree that's the case here. I'm very happy to accept technical answers, since I can always retrace it to the basics.

By "we" do you mean nature or medical intervention?

"we" age due to nature...?

@TheLast_Cipher Excuse me, I meant when you said "why not catabolize DNA and replace it". My point is, are you asking why we've not evolved to replace our DNA or whether we could use DNA replacement as a medical therapy.

@Jam: I am asking why we have not use DNA replacement as a medical therapy.

It seems very feasible to synthesize human DNA (please inform my
  ignorance, if I'm wrong. lol.) and it looks very promising after
  reading this:
  https://www.wired.com/story/live-forever-synthetic-human-genome/.

It is certainly possible to synthesize human DNA, but it's another thing to create a functional chromosome. In fact, in the article you link to, they are discussing a research effort to synthesize a human Y chromosome. As far as I can tell they haven't actually done this yet, they are just proposing to attempt it. George Church is a highly regarded genomicist, but the article is very sloppy about distinguishing what they think they can do from what they've actually done. There has been work with human artificial chromosomes (HAC), but these have been special purpose constructs that successfully replicate and divide in cells, but don't duplicate an entire natural chromosome.
Synthesizing a human genome would just be the start of the therapeutic process. You then face the question of how to place the synthesized genome in the cells of the recipient. Current approaches to gene therapy involve inserting a single "repaired" gene into a virus, and then infecting the relevant tissue with that virus. This doesn't insert the gene into all cells of the body, just the ones infected with the virus. For some simple genetic diseases this is enough to relieve the symptoms of disease. You can't insert an entire human genome into a virus though.
It's also been proposed to harvest stem cells from the recipient, modify them with the repaired gene, and re-insert them in the diseased tissue. Again this would affect only a portion of a single tissue, not all the cells of the body. It's also one thing to insert a short sequence into a stem cell, but nobody knows if you could swap out a stem cell's entire genome and still maintain it as a stem cell. Also, this would only work for tissues that are still actively dividing. Many important tissues (in the brain for example) have stopped dividing or divide only slowly in adults.
Even gene therapy involving single genes has been approved in only a handful of diseases. It's sill almost entirely experimental. What you are suggesting is still in the realm of wild speculation. Speculation can be inspiring and motivates research programs, but don't starting counting chickens yet.

Is it correct to say that a DNA becomes a functional chromosome only when it is in an environment where it can be transcribed and replicated? So delivery methods are just as important?

@TheLastCipher it's even more complicated than that. Our chromosomes are complex structures with the DNA wrapped around a trellis-work of histones and other proteins. The 3-d structure of the chromosomes plays an important role in the regulation of gene expression and is controlled in turn by a hundreds of proteins coded in the DNA.

I would like to encourage further discussion so I'll retract the acceptance of your answer. Hope you don't mind.

@TheLastCipher you're welcome to retract the acceptance of the answer and vote it  up or down as you see fit. However do note that StackExchanges is intended to be a question and answer site, not a discussion forum, ala Reddit or many others. If you would like an open ended discussion on a topic you can open a chat room once you have enough points.


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Does loss of dopaminergic neurons totally eliminate voluntary muscular control?
Breathing is a function that is not only autonomic, but can also be temporarily overridden and placed under voluntary control. In fact, you are now breathing manually. Now, suppose that someone has completely lost the ability to voluntarily control his/her muscles due to destruction of the brain's dopaminergic neurons in the substania nigra (such as due to Parkinson's Disease or MPTP poisoning). This would normally result in total paralysis of voluntary muscles and inability to move. Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically? What about defecation (Which requires one to voluntarily relax the anal sphincter)? What about rolling the eyes?

"Otherwise the person is totally fine" is very inaccurate and does not describe Parkinson's. I do think there is an interesting question here but it would be better separated from this bizarre scenario.

No it would eliminate only fine motor control; Patients with parkinsonism are not paralysed as much as loss of fine movement they have spastic movement...

Suppose that someone has completely lost the ability to voluntarily control his/her muscles due to the destruction of the brain's dopaminergic neurons in the substania nigra
This is not correct. The substantia nigra plays an important role in both reward and movement. The degeneration of dopaminergic neurons in the substantia in Parkinson’s disease leads to loss of fine motor movement (leading to limited movement and tremors) and some loss of non-motor skills (loss of smell).
What locations control breathing?
The autonomous regulation of breathing is controlled by bundles of neurons called the dorsal respiratory groups (DRG) and ventral respiratory group (VRG) that together make up the medullary respiratory center. Source.

Though the exact mechanism of how we control our voluntary breathing is still a debated. We have a general idea:

Voluntary control of breathing is mediated primarily via the
  corticospinal and corticobulbar tracts and is important in activities
  such as speech, singing, and voluntary breath-holding. Disorders
  involving this mechanism occur mainly in bilateral pontine infarctions
  and lesions involving the pontine tegmentum that interrupt the
  descending motor pathways. - Neurology and Clinical Neuroscience, 2007

Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically?
Although the exact mechanism for voluntary breathing is not fully understood, the voluntary process is controlled by a series of nerve bundles. If the nerve bundles were severed, there would be decreased voluntary control over the breathing process. Losing the ability to manually breath could be bad for overall health. One study has found that a lack of the ability to manually breath can lead to poor spinal stabilization and posture.
What if you lost autonomous control?
There is a rare disorder known as central hypoventilation syndrome (CHS) that results in respiratory arrest during sleep (also known as Ondine's Curse). This disorder is caused by a lack of development of the neural tube (aka Medulla and the VRG/DRG) during birth or some type of traumatic brain injury. Treatment for this disorder is a lifetime of mechanical ventilation.


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Cross species effects of Apis mellifera queen pheromones
I am looking for studies that show effects of Apis mellifera queen pheromones on other species. An example of one such study is where A. mellifera queen pheromones deactivated the ovaries of Drosophila melanogaster females. Similarly queen pheromone from Apis mellifera scutellate can deactivate worker ovaries in a different sub- species, Apis mellifera capensis (however, this is a sub species effect and not cross species). If anyone else knows any other studies of cross species effects, it would be highly appreciated if it could be pointed out.


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Passing out from drowning
How long does it take to pass out from oxygen deprivation? The person is panicked and screaming so they accidentally breathe water into the lungs. So how long would it take for them to pass out? After they pass out they are administered Mouth-to-mouth resuscitation immediately and are only out of it for a couple of half a minute. Then they are taken to the hospital. Would there be any long term affects to the body?

A couple of half a minute? Anything under 5 minutes is a 90% chance of being safe if resuscitated. Drowning people don't make much noise because they are too distracted by the water. They only fill their lungs significantly after becoming unconscious.
simple description:
https://www.dedhamhealthfoundation.org/water/victim-recognition/stages-of-drowning/
complex description:
https://en.wikipedia.org/wiki/Drowning#Pathophysiology
The damages that occur are: lung injury, cardiac arrest, brain injury from oxygen deprivation.
The breathing pattern and physiology vary depending on hyperventilation, panic, physical exertion, fullness of the lungs at the time of submersion, so there is no simple answer to your query.
When they breathe significant amounts of water, it is because they have just lost consciousness and their body relaxes.
While they are is still conscious, they hold their breath for as long as they can, voluntarily / because they have breathed a sip of water and their epiglottis shuts and seals closed, by reflex.
There is a spasm called laryngospasm which occurs when the person is at the end of their breath and their body is trying to breath but their epiglottis is closed, that occurs at very low oxygen levels and a high oxygen debt because of the panic, so unconsciousness is only a few seconds away when the throat is convulsing, and it continues to convulse when they are unconscious and 90% of the time they breathe water and their heart continues beating.
I can't find how long it takes to have cardiac arrest after asphyxia or wet drowning. Probably it is not very well studied becuase it is so dangerous.
There is also the mammalian dive reflex, which occurs mostly in children who are suddenly immersed in freezing water. It can cause their metabolism and heart rate to go into slow motion, and stops circulation to their extremities, causing them to survive for more than 15-30 minutes.

This is a kayak trip heart rate with immersion in cold water.
From avalanche asphyxia, the heart can continue 15-20 minutes:
https://www.scancrit.com/2013/08/27/heart-rate-monitor-watches-avalanches/
There's a dutch man who lost his wife and then started diving in freezing water, and he can stay in freezing water for 30 minutes using conscious mammalian dive reflex.


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Worm Identification
Please identify the attached worm and larvae.
Location:  Payette, Idaho
Approximate size:  1 mm
Found in home.

Note:  I have photos of dozens of these, "things."  The samples were gathered using a lint roller.  They are on my bed.  I use a $20 lens with a USB port to my laptop camera.  I am unsure of the magnification.


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Is it better to receive a certain dose of radition gradually or all at once?
Suppose you had to choose between getting exposed to 1000 mSv gradually over the next 5 years, or all at once exactly 5 years from now.
Which one would be the healthiest option? Is the probability of having developed a disease like cancer after those 5 years the same in both cases?
Phrased differently: Are the effects of multiple doses of radiation entirely probabilistic and/or cumulative?
Thanks in advance!

The period of time over which a dosage is given matters critically. You probably have experienced this in your daily life. If you are out in the bright, summer, sun for 8 consecutive hours on a single day, you are likely to get a sunburn. If you are out in the sun for a total of 8 hours spread evenly over a month, you're very unlikely to get sunburned.
You body has mechanisms that can repair radiation damage or limit it's effect, but these processes take time. A particularly important processes is apoptosis. A cell can detect if its DNA has been critically damaged, and self-destruct before something else goes wrong. If the exposure is acute, there my not be time for the apoptosis mechanism to take effect before it is damaged itself, possibly transforming the cell into a cancerous state. There is considerable evidence that lower dose rates do give rise to fewer cancers.


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Why are worms, centipedes and snakes long?
Some animals have mostly distinct, non-repeating body parts, each performing a particular function. However, some kinds of animals, such as worms, centipedes and snakes, have a long body that appears to be longitudinally uniform in most of its length. What is the evolutionary sense to that? For instance, what advantage does having a hundred of limbs convey to a centipede, while a spider is happy with a tenfold less?

We have an ontogenetic answer (the Oct4 gene is responsible for the continued growth of snakes), but it doesn't look like we yet have any good explanation for why it has happened. My take would be for the way snakes have been feeding. It helps them by having longer stomachs that can accumulate more preys in one hunt, then they can rest for a while.


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How does the strength of 3D printed tendons compare to original tendons?
There have been some attempts such as {1,2} to 3D-bioprint tendons. How does the strength of 3D-bioprinted tendons compare to original tendons? I am mostly interested in human tendons.

References:

{1} Ede, David, Nikki Davidoff, Alejandro Blitch, Niloofar Farhang, and Robby D. Bowles. "Microfluidic Flow Cell Array for Controlled Cell Deposition in Engineered Musculoskeletal Tissues." Tissue Engineering Part C: Methods 24, no. 9 (2018): 546-556. https://doi.org/10.1089/ten.tec.2018.0184
{2} Rimann, Markus, Sandra Laternser, Hansjörg Keller, Olivier Leupin, and Ursula Graf-Hausner. "3D bioprinted muscle and tendon tissues for drug development." CHIMIA International Journal for Chemistry 69, no. 1 (2015): 65-67. https://doi.org/10.2533/chimia.2015.65 (open access)


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Cardiac vs. skeletal muscle contraction
For the heart muscles, it is the extracellular Ca2+ that is necessary for the contraction, but for the skeletal muscles, it is intracellular Ca2+.
One of my answers on a test was the following: "In cardiac muscles, an augmentation of the intracellular Ca2+ concentration is necessary for muscle contraction".
Therefore, I'm confused. For the heart, is it extracellular or intracellular Ca2+ that determines contraction?

Perhaps your confusion will be helped by separating for you 2 processes that occur in both skeletal and cardiac muscle contraction.  The first process is the electrical change (action potential) in the muscle cells membrane that triggers the contraction and the second is the contraction of the muscle cell itself.
The latter process, contraction of the muscle cell, is basically the same for both muscle types.  Simplistically this requires high intracellular Ca in both skeletal and cardiac muscle.  In short, when the intracellular Ca in the cell is high all muscle cells will contract and when it decreases they will relax.
The difference between the cell types is what triggers this increase in intracellular Ca when the cells are stimulated I.e. what causes the increase in intracellular Ca.  In skeletal muscles the action potential moving through structures called t tubules directly causes release of Ca from the sarcoplasmic reticulum.  In cardiac muscle this is different as the action potential here causes Ca to enter the cell from outside and it is this small amount of Ca coming from the extracellular space that triggers release of the far larger amounts of Ca in the cell that are needed for contraction.  This is called Ca Induced Ca Release or CICR.
Schematic pictures are the best way to understand the differences in the processes in the 2 muscle types so try these 2 links (Cardiac (https://courses.lumenlearning.com/boundless-ap/chapter/cardiac-muscle-tissue/) & Skeletal (https://opentextbc.ca/anatomyandphysiology/chapter/10-3-muscle-fiber-contraction-and-relaxation/)
You can also access the Textbook of Medical Physiology by Guyton and Hall online or at a school/university library which will give you more detail.


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How does a nerve cell adjust if O2 diffusion is interrupted?
What effects would it have on a nerve if the oxygen supply is cut off? Is there any data on this?
Does the nerve conductance velocity increase? What about the Amplitude and receptor-channels on/in the nerve?
Funnily enough it's insanely hard to come by an answer to this question, or maybe I'm just searching at the wrong places....

There should be plenty of studies on this topic. At least it is quite a well known fact that brain is one of the first organs to be affected by of oxygen deprivation.

If Oxygen diffusion is interrupted, there is a serious problem. Neurons inside of the brain slowly start to die, many other things like change in personality or the inability to process pain impulses occur if the brain is deprived of oxygen.If this is not fixed within 15 minutes it is impossible to survive.
The actual effects on the neurons are as follows:
Like in most cells the first solution to this kind of circumstance is anaerobic metabolism, the same happens in neurons but it does not last long and it is inefficient. As far as i'm concerned nerve conductance decreases in this kind of scenario and the receptors shrivel.
Well if the receptors are shriveling, they shouldn't be able to transfer impulses meaning that nerve conductance should stop.
This link to an article on the effects on the brain from oxygen deprivation.
https://www.livestrong.com/article/106179-effects-lack-oxygen-brain/

Thanks, that's what I was also thinking, I'm gonna leave the question open for a bit longer, maybe somebody can add more information, hope you don't mind.

Brian, it would be great if you can add some references to support your answer and explain a bit on how lack of oxygen affects the conductance. (Hint: ATP synthesis, Na/K pumps, Neurotransmitter release/re-uptake).

@WYSIWYG please elaborate, all I can find are general impacts on the whole human, not a single cell lol

@schokakola then I can write a new answer myself. I need some time for it. Brian is almost there. But there needs to be better referencing.

@brian please try to cite more authoritative references like peer-reviewed articles or books. Blogs are just slightly more than opinions. They are not rigourous and can miss important details. You need to find articles on effects of hypoxia on neurons which is not a very difficult to search topic. Also, you haven't taken my hint on the effects of loss of ATP on different neurological processes.

Ok I will try to find some better references and talk bout ATP synthesis.

By the end of tomorrow I will try to complete my explanation.

Also thanks for the feedback on my answer

lol thanks , also i don't care about citations, i just want to know whats true

@schokakola it does not matter whether you care or not. Citing proper references is essential as per the site policy. Answer are not supposed to be just for the satisfaction of one user; it should be useful to anyone who wants to know about the particular topic.


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What problem does the Dobzhansky-Muller Model resolve?
This page describes the Dobzhansky-Muller model and I can follow the illustration of the split leading to incompatible hybrids.
But at the start of the page the author states "[Dobzhansky and Muller] both realized that hybrid inviability or sterility was unlikely to arise from a single change at one locus." I don't really understand the explanation that follows i.e. what exactly is the issue with having a single change at one locus?
I wonder if someone here could explain the issue more clearly.

If reproductive isolation was to be caused by a single mutation, then the first individual to carry this mutation would likely have a very low fitness. At the extreme, in a purely sexually reproducing species without hermaprohiditism, this individual carrying the first mutation causing reproductive isolation would have no-one to reproduce with and would have a fitness of zero.
Hence, reproductive isolation is unlikely to arise from a single mutation as these mutations are unlikely to raise into appreciable frequency. Hence, Dobzhansky and Muller (and Bateson) created this minimalist model involving only two loci with negative epistatic interactions.


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Where does this equation in the electrophysiology literature form come from?
In my studies I keep coming across the form of an equation that is used in many different mathematical models for voltage gated ion channels. The most general form I have found is in the 1977 paper Reconstruction of the action potential of ventricular myocardial fibres by Beeler and Reuter. Each ion channel has a gating variable $y$ whose differential equation depends on functions $\alpha$ and $\beta$, both of which take on the general form:
$$\{\alpha,\beta\}=\frac{C_1\exp[C_2(V_m+C_3)]+C_4(V_m+C_5)}{\exp[C_6(V_m+C_3)]+C_7}$$
where $V_m$ is the membrane potential and each constant is determined to have different values depending on the channel, system, etc.
My question is where does this form come from? In all of the papers I have come across they seem to just use this form with numbers chosen to fit their data without explanation as to why this form is actually used. The Beeler and Reuter paper cites the 1952 paper by Hodgkin and Huxley, but it seems like H&H use simpler forms of this equation primarily motivated by just fitting the data rather than illuminating any underlying mechanisms. Therefore, I do not understand where this form in the B&R paper comes from that so many papers later on use as well.
Does this form come from assumptions about the workings of the ion channels, if so, what are these assumptions, and how do they give rise to this form? Or is this just a general form found to fit many data sets fairly well, and if so why was this chosen over other functions that could probably do the same thing?

They chose that equation mainly because of numerical simplicity. It can fit the rates $\alpha$ and  $\beta$ for all the ion channel particles in the model.
The theoretical foundation for the equation, as in the H&H model, are loose. It resemble the equation derived for the movement of a charged particle in a constant field. But it is not an equation derived from the ion channels biophysics. We can't blame them, considering that at that time (1952) they don't even know for sure that ion channels where proteins.
In page 183:
 In order to simplify the reporting of the actual values used in this model, we have expressed the alphas and betas entirely in terms of a generalized function, with eight defining coefficients. Table 1C gives the equation, and the defining coefficients for al rate constants.
For the generalized function note that in every case at least some of the coefficients are zero: this generalized formula is just a way to collect both possible forms for the H&H rate constants.
I have read papers using Eyring equation for a theoretical formulation of transition rates, based on thermodynamics.

This is partly true, in that in the HH model the theoretical foundations are at best loose, but I would not say they are non-existent: they refer to Goldman for example and all relate to Boltzmann equations. The choice of the generalized function in the Beeler and Reuter paper is mostly motivated by algebraic simplicity. That said, all are approximations to more modern biophysical models.

Goldman equation refers to the ion reversal potential not to the ion channel dynamic. $\alpha(V)$ and $\beta(V)$  are not Boltzmann function in H&H model. As far as I know, they are just phenomenological. If you know any derivation for them please let me know.

@heracho Bryan isn't referring to the Goldman equation. I think a paper by Goldman in 1944 is being referred to, which is cited by the HH paper when discussing a lose physical interpretation of their equations for $\alpha$ and $\beta$

@BryanKrause Are the biophysical models these are based on just as explained in the HH paper of a charged particle moving in a constant field? Or are there other models you are referring to?

Basically HH compare their results to Goldman's results for a charged particle, i.e. an ion moving across some boundary; they note that their equations similarly evoke a charged something moving within the membrane, which is both a fairly accurate if abstracted notion of what really happens now that we have fuller models of ion channels, and also makes a whole lot of sense for how you could implement a biological ion sensor. So to @AaronStevens "Are the biophysical models these are based on just as explained in the HH paper of a charged particle moving in a constant field?" - Yes.

@BryanKrause  Thanks for the hint. In H&H 1952: "First, it is one of the simplest which fits the experimental results and, secondly, it bears a close resemblance to the equation derived by Goldman (1943) for the movements of a charged particle in a constant field. Our equations can therefore be given a qualitative physical basis if it is supposed that the variation of $\alpha$ and $\beta$ with membrane potential arises from the effect of the electric field on the movement of a negatively charged particle..."

@heracho Yeah, that's the sentence I was referring to; they also talk about how it doesn't quite fit Goldman (I think in the next sentence, or maybe next paragraph), because the voltages that they fit are not symmetrical. They basically punt and say "we don't know what exactly is going on" which is pretty fair given they are writing this in the 1950s (fair enough for a Nobel prize at least ;) ). I think if you add this comment discussion to your answer and summarize this comment discussion a bit it would be a good answer.

@BryanKrause, I edited trying to summarize the discussion. Please feel free to edit further.


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Vegetation Monitoring - Why permanent plots
Why do most vegetation monitoring programs rely on permanent plots?
Take the context of a single ecological restoration site, for example.  Let's say the variable of interest is cover by plant species, and monitoring is conducted throughout several seasons to track the relative/total cover of multiple species.
If plots are randomly sampled within homogeneous vegetation assemblages, why not just establish new plots each sampling period, rather than locating and re-sampling the same plots over and over again?
If the goal of sampling the is to represent characteristics of the population (i.e. the homogeneous area of vegetation), then why do researchers always sample permanent monitoring plots again and again rather than using a new set of randomly selected plots each time?

Are you asking in the context of a single longitudinal study using particular plots, or in the context of multiple separate studies over time?

A single study area.  I will edit my question to be more clear.

The answer boils down to statistics rather than anything particular about this type of experiment.
If you have a sample of plots, and then take repeated measurements in that same sample over time, the variance in the values you record is a function of the variance of the time-dependent process causing changes.
If you take future measurements from a new sample of plots, you have additional variance to account for due to choosing a new sample. That is, even if you would have measured no change at all in the same plots, you expect the second sample will be different from the first just because of sampling. Because of this additional variance, you have less ability to detect smaller changes over time: less statistical power.


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If we can make magic bullets that are basically artificial antibodies, why has a cure for cancer not yet been developed?
So protonsil and salvarsan 606 where both used as the first magic bullets in the modern period of medicine in the 1900s. However, if we can create artificial antibodies that target specific diseases how have we not come up with a cure for cancer? It seems it shouldn't be that difficult. But if we COULD create artificial antibodies that target cancerous cells would we be able to do it effectively without the drug having any bad or quite noticeable side effects on the body?
By the looks of it chemotherapy is the closest we have gotten so far in chemical drugs, but it does have some nasty side effects.
I was aware of 5 of the approved treatments.
However each type of cancer is similar but different, would it be ever possible to create a generic treatment?
Edit: I have found something interesting, scientist have come across a way to change the antigen on a cell however it is not fully understood.

The Wikipedia article on cancer immunotherapy includes 9 different US FDA-approved anti-cancer antibody treatments. Can you clarify if your question is because you were unaware of these treatments or if you have some other question?

Adding to @BryanKrause comment: These therapies often show spectacular results in the patients where they work, but it is not yet understood, why they don't do this in all the patients.

To over-simplify is bit, the problem is that cancer is not caused by foreign agents like bacteria or viruses, it is caused by a small change in the body's own cells.  It's thus very difficult to create antibodies that recognize the cancer cells as "foreign".

This is a good question.
The first answer is that there are antibody therapeutics for cancer.
These fall into two categories which I will call therapeutic and immunotherapy (this is not typical naming but, keeping it simple they will do).
Therapeutic antibodies are designed to bind to an enzyme or signalling protein that will weaken the tumor specifically.  An example is an antibody to nutrient intake receptors (cancers eat a lot more than other cells). HER2 is a receptor that is heavily populated on breast cancer tissue.  Antibodies that inhibit HER2 activity can slow the growth of breast cancer specifically with minimal toxic effects.
There are also antibodies to proteins found only on cancer cells.  These can be specific antibodies (monoclonal antibodies) to proteins from a mutation that only the cancer cell has.


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How do painkillers prevent shock?
I was reading about the Placebo effect and came across this little story:

The roots of the placebo problem can be traced to a lie told by an
  Army nurse during World War II as Allied forces stormed the beaches of
  southern Italy. The nurse was assisting an anesthetist named Henry
  Beecher, who was tending to US troops under heavy German bombardment.
  When the morphine supply ran low, the nurse assured a wounded soldier
  that he was getting a shot of potent painkiller, though her syringe
  contained only salt water. Amazingly, the bogus injection relieved the
  soldier's agony and prevented the onset of shock.

https://www.wired.com/2009/08/ff-placebo-effect/
I also read that Morphine specifically lessened the effects of shock:

Only when it is severe, or when a severely wounded or injured person must be moved quickly (as from a wrecked vehicle or aircraft) it is wise to give Morphine at once. It may not always relieve the pain entirely, but will certainly lessen shock.

https://web.archive.org/web/20140420133119/http://www.med-dept.com/morphine.php
So, how do painkillers prevent wounded soldiers from going into shock and dying? What physiological mechanisms are responsible? Is it something to do with blood pressure? Heart rate? Pain itself?

A little clarification: what exactly do you mean by 'shock'? In modern medical terminology, it means a state of generalised tissue hypoperfusion. In days of old, it was often used for what is now called an acute stress reaction (which is a psychological phenomenon rather than a physiological one). Which one do you mean here?

1) Pain can aggravate hypotension, so painkillers may help to prevent shock.
A severely wounded person with significant blood loss can develop hemorrhagic shock due to drop in blood volume and consequently drop of blood pressure and insufficient perfusion of vital organs.
It is known that pain can trigger vasovagal syncope, also known as neurocardiogenic syncope in which a person faints due to sudden drop of heart rate and arterial vasodilation resulting in drop of blood pressure and reduced brain blood perfusion.
Here is an example how carbamazepine, which prevented pain, also prevented the episodes of neurocardiogenic syncope (The Korean Journal of Pain):

A 65 year-old male patient diagnosed with glossopharyngeal neuralgia
  complained of severe paroxysmal pain in his right chin and ear
  followed by bradycardia, aystole and syncope. We report a case
  successfully treated with a permanent pacemaker and carbamazepine in a
  patient with GPN who had syncopal attacks preceded by paroxysms of
  pain.

In an injured person who is at risk to develop hemorrhagic shock, severe pain could cause neurocardiogenic syncope that could proceed into shock, so, it sounds logical that painkillers could help to prevent shock.
From the first quote in the question (the patient was convinced he was receiving a strong painkiller), we cannot conclude that the painkiller prevented shock, because this has not even started to develop.
2) Analgesics for a person in severe pain who has lost blood and is in danger of developing shock.
According to Pain Control in Trauma Patients (Trauma Reports, 2011, fentanyl can be appropriate painkiller in shock since it does not aggravate hypotension:

Fentanyl is the best known synthetic agent and is widely used in pain
  control. It is 50 to 100 times more potent than morphine and has the
  added benefit of not causing histamine release and peripheral
  vasodilation, as found with morphine administration. Based on this
  physiology, fentanyl should not impact blood pressure as much as other
  narcotics and, therefore, is preferential in the critically ill trauma
  population who may have tenuous cardiovascular status from hypovolemic
  shock.

Morphine can cause hypotension, so it may aggravate shock. According to prescribing information for morphine sulfate oral solution by FDA.gov, 2018:

In patients with circulatory shock, Morphine Sulfate Oral Solution may
  cause vasodilation that can further reduce cardiac output and blood
  pressure. Avoid the use of Morphine Sulfate Oral Solution in patients
  with circulatory shock.

In conclusion, painkillers may help to prevent shock by reducing pain.

This answer is factually incorrect. It makes an incorrect connection between vasovagal syncope and shock. The two are fundamentally different entities.


text:
Can GENESIS simulation software be adapted to other types of tissues?
GENESIS simulation software http://genesis-sim.org/ is designed for neurobiological systems and it is able to inculude in the simulation the different resolution levels - starting from the molecular interaction and ending with neuronal interaction. My question is - can GENESIS be applied to other tissues, are there efforts to do this and what kind of adaptations should be made? I guess that GENESIS is already capable to include full diversity of the molecular interaction patterns that are common to all cells. But some tuning is necessary for models at the cellular and multi-cell level? I guess that there is lack of dedicated GENESIS-level software for other tissues and systems.

Perhaps you can "switch off" the specific neuronal pathways to simulate a normal cell. However, I cannot comment much without knowing the details of the model used in the software. However, you can try this software called virtual cell. It also allows importing different models created by different people, from a repository.

I'm only vaguely familiar with GENESIS but can't imagine using it for non-excitable cells, since the core is the differential equations you use to simulate membrane potential. You could certainly use it for other excitable cells like immune cells to study just those properties, but if you were interested in, say, muscle, you'd probably want a whole other set of dynamics not incorporated. Maybe they've added more detailed molecular interactions since I looked last and maybe you can provide a more specific link to what you are thinking about so we don't have to dig through the docs.


text:
What’s the name of this tree?
I’m trying to find information about this tree that I didn’t plant. Looking for information in terms of pruning, etc.

It had white flowers on it this spring, but is now flower less and has very few young berry-esque type fruits growing on it. They’re very small still, but it seems they’re going from green to a red. This in Michigan.
Additional pictures:

Thanks to Bryan Hanson for the answer! Found a picture online of it with flowers:

Where is this plant located?

Could you please add close-ups of the leaves, flowers and fruits?

@Chris Michigan. Sorry I should have included that in OP. I will upload closer pictures sometime today when I return home.

@Taskle please [edit] your own post to include your location as well as additional close-up images of the leaves and fruit. The more detail the better!

I've added additional pictures, with closeups on the leaves as well as one of the fruits. I can really only count 2-3 fruits growing as of right now on it.

Revised Answer
The additional pictures point to something in the genus Prunus.  Note that there are extrafloral nectaries at the base of the leaves, and feathery stipules are visible (see here for annotated picture of a different species).  Since it has a weeping habit, and doubly toothed leaves, I think what you have there might be a Japanese Weeping Cherry Prunus subhirtella var. pendula (but other names seem to be in use).  Some info here which seems consistent with your specimen.
Original Incorrect Answer
I think you are probably looking at Ulmus glabra "Camperdownii" or a similar cultivar.  This is a "weeping" elm variety that is produced by grafting; all plants are descendants of a single tree. Wikipedia gives the full background.  Your specimen has somewhat more pointy leaves than many of the images for Camperdown Elm I found online, but apparently there can be some variation.
EDIT: The fruit picture (added after my answer) clearly rules out my answer!  Also looks like there are nectaries at the base of the leaves.

The Japanese Weeping Cherry is definitely it. I found some pictures online and the “snow” colored flowers are a perfect match as to what it looked like back in April.


text:
Why do we need to diversify our food sources to live healthy, where other animals live happy on one source?
We read about eating different food to get all vitamins and minerals our body need, and often you find people fail to get the daily amount of a certain thing.
I wonder why we humans need to do this where other animal live fine on grass only or leafs only

All organisms have some dietary requirements. Many organisms cannot synthesize everything they need from basic compounds and they have to obtain them from other organisms. This is not specific to humans.

OK, What about sheep as an example, do they eat anything other than grass? Does grass has all the nutrition they need?

Strictly speaking, humans, at least infants, can live on a single food source - milk. The current recommendations about eating something from all food groups may be exaggerating. Several studies have shown that vegans are not of greater risk of developing disease than omnivores, for example.

You say that like grass or leaves are easy to live off of, animals that live off these materials have highly specialized digestive systems to extract enough nutrients from it. Also note these herbivores are more than willing to eat things like meat and eggs when they can get it. Deer will stomp nesting birds to death and eat them. They can improve their health by obtaining these nutrient rich sources.

Also, grass and leaves are not simple things, but are quite diverse.  E.g. many humans happily consume the leaves of lettuce & cabbage (and other sorts like grape leaves in regional cuisines: https://en.wikipedia.org/wiki/List_of_leaf_vegetables ), but would be poisoned by eating the leaves of say rhubarb.


text:
Will daily sweeped ants eventually learn their path is a dead-end?
An ant colony (likely Lasius niger) made its way through one of our rooms, literally.  That is, they enter by a door and leave by the other, and vice versa.  Some carry eggs, but in both ways, so I'm not sure whether the nest is on one side or the other.
I sweep them outdoor everyday, but each night they repopulate the path.  Am I wasting my time or is there a chance sweeping makes them decide it's a dead-end ?
NB : Washing the floor didn't change anything.  I also tried to barricade with somehow large amounts of essential oil of Eucalyptus citriodora, but it didn't seem to help.  Anyway although suggestions to get them leave are welcome in comments, I'm genuinely interested in knowing if the sweeping strategy may have an effect or not.

Related : https://biology.stackexchange.com/questions/20431/can-ants-learn-things

I often trace the trail as far as I can away from my home and plant bait poison in line with their current path. I then use vinegar to scrub their path everywhere beyond the bait trap. The ants enjoy this new closer food and usually seem unable to find their way back into my home


text:
What does "count in gene set" mean?
I am trying to understand the analysis generated by STRING.
In analysis for biological processes table, there is a column titled "count in gene set." This gives a value for example "68 of 498".

What does this refer to?

It means the software has 4753 genes it has labeled with "biological regulation" and the short list you gave has 45 of those genes.  That is a little higher than you might expect by chance if you'd given a random gene list of the same size.

2.94e-06 FDR suggests to me it is significantly higher than you might expect by chance.


text:
Help identifying a weird creature
Okay, so there is this weird creature, which has been crawling around our house.
I can hear it moving around, and it's especially active in the dark. I've however been able to take a picture of it.
If it helps, it's a carnivore (I've thrown some hot dogs and such).
This weird thing is 25-30cm long, and the picture of it was taken from a balcony on the second floor. I've only been able to photograph it once, but never came close to it otherwise. We live in central Europe, in a small town that somehow resembles a village. As for the ecosystem, I don't quite know. Fields, rivers and forests are all in proximity of our house.
Thank you for your anwsers,

Can you please add more information? What is the approximate size? Where do you live (country, region, type of ecosystem, urban or rural, ...)? How close did you get? Did you take this picture from two meters away, from a window at the second floor, ...?

The black and white colours on the front and the grey back as well as the overall shape make me think it could be a badger. Given the location, it could be the European badger (Meles meles). The size matches, and badgers are omnivorous, so they can eat meat.

It looks most like a hedgehog to me.  If you want to encourage a hedgehog, a bowl of fresh water is always important, and some cat food.  If you see a hedgehog in the day time, it is possibly in distress.


text:
Why do we find flowers attractive?
Given that we (humans) are not evolutionarily closely related to bees, why do we find flowers attractive?

Attractive to what sense, sight or smell?  Quite apart from individual preferences, there are some which have repulsive odors (notably Rafflesia, which is said to smell like rotting meat: https://en.wikipedia.org/wiki/Rafflesia ), many others which have an inconspicuous appearance.  Also note that many garden flowers have been selectively bred to be more attractive to humans than their wild progenitors.

I meant sight and, sometimes, smell.

Sure, flowers can be sign that the fruit is underway as @JonathanMoore said and viewing any trait as a result of selection is probably what the OP was waiting for. Thinking that if an organism produces a behaviour, then this behaviour must have been selected is wrong though.
The reality is that specific behaviours are affected by evolution of other behaviours and other traits as well as an by our environment (incl. social environment). It will be particularly difficult to hypothesize as for the different selection pressures that may have existed on a specific behaviour especially in animals with such high cognition as humans. Maybe we like flowers because we like colour contrast and maybe we like colour contrast because face with stronger colour contrast is more attractive because it is a sign of health. Maybe we like sunset because we like flowers. Maybe we like colour contrast because we like fresh fruits. Maybe, we like complex design because it makes us think about the possible complexity of shapes. Maybe we like complex shapes because we like to explore. Maybe we like simple design because we like clear skins. Maybe we like flowers because of the diversity of shapes. Maybe we like flowers because they are a sign of the end of the cold winter. Maybe we like flowers because we are being told that they are pretty things. Maybe we like flowers because it symbolizes abundance and reproduction. Anyone could formulate loads of hypotheses. Maybe we like flowers because we like any smell that is not the smell of something that is rotting. Maybe we like flowers because we like trees, leaves, mountains, rivers, lakes and pretty much anything else in our natural surrounding. Maybe we like flowers because flowers is a sign that there is not no pests in our garden or simply that the plant we are growing is healthy.

Re "...any smell that is not the smell of something that is rotting", there's for instance Fritillaria imperialis https://en.wikipedia.org/wiki/Fritillaria_imperialis which, while it's a striking flower, smells rather like a skunk.  Or some kinds of Iris which smell nice (to me) in moderation, but are rather sickening in quantity.

Flowers are a sign that fruit is on its way, so it would be advantageous for us to remember the place where we saw flowers.


text:
Does the frequency discrimination of the outer hair cells of the ear increase with sound pressure?
I'm wondering whether the frequency resolution of the inner ear increases/decreases with the volume level (caused by sound pressure $(N/m^2)$.
My assumption would be that as long as the pressure level is high enough to cause a pressure wave in the scala media/corti-organ, the frequency discrimination has nothing to do with the volume level.
There doesn't seem to be any information regarding this question!
Let me give an example to illustrate better what my question is:
If I have a sound with $20 \ dB$ and a certain frequency $1000\ Hz$ will the ability to judge the note (frequency) increase or decrease with the pressure?

Do you mean the inner hair cells?

lol no, i think they are called outer hair cells; also there are inner hair cells and outer hair cells, the outer ones are responsible for frequency discrimnation, so i want to know whether or not that depends on the pressure/volume or not or if there is a optimal pressure level where frequency discrimination is the ighest

The outer hair cells are "motor" cells, mechanical amplifiers. Inner hair cells are the ones behind perception (aka frequency discrimination). You still could really mean the outer hair cells, because they also respond to sound, but their function is to modulate the response of inner hair cells. Also, why are you differentiating between volume and pressure (do you mean to?) A 20 dB 1 kHz sound is a sound of a specific volume; if you change the pressure it is no longer 20 dB.

Well I found an answer: the optimal range (highest possible frequency discrimination) is supposedly at $1 dB$ so it does not increase with soundpressure/volume


text:
Why did T cells have evolved to recognise self cells along with foreign antigent to generate a response?
T cells have evolved to be strain specific. For a T cell to respond it has to identify not only the foreign antigen but the antigen must also be attached to a self cell. what is the significance of that? Isn't that the reason behind autoimmunity and hypersensitivity? I understand about foreign antigen, but why self cells? the experiment by Zinkernagel and Dorothy about MHC restriction shows that same antigen presented by a foreign cell will not be killed by sensitized T cells.

Your question is unclear. "For a T cell to respond it has to identify not only the foreign antigen but the antigen must also be attached to a self cell", not really. The antigens have to be presented to the T-cell via the MHC. Can you please clarify?

yes, the antigen is presented by APCs via MHC, but there's a condition to that, the said APC must be a SELF cell, and T cells have to identify that the antigen is presented via a self cell only, otherwise there will be no reaction or killing or response. i mentioned an experiment in mouse by Zinkernagel and Dorothy. i am confused why cant a T cell simply kill the foreign antigen presented on the TCR  via MHC, why must it also be on a self cell. recognition of self cells is one of the causes of autoimmune diseases, so why did T cells evolve to be that way?

So please [edit] your question to clarify this. Comments are easy to miss and are not searchable. Also, add a link to the research you mentioned.


text:
Type of Tree With Somewhat Squarish Fruit
I live in the SF Bay Area and am trying to identify a tree on my street. It's the fruit that is confusing me -- does anyone know what this fruit is?
It's not a rare tree -- there are at least several more on the surrounding streets.
Mature leaves are about 6" long and greater.

Could you put something in to indicate scale?

Looks like the regional government maps every street tree: https://data.sfgov.org/City-Infrastructure/Street-Tree-Map/337t-q2b4 Maybe you can find it!

A photo of the bark/trunk would be useful too, and if you can break off a leaf and see if there is any latex that oozes out of the wound.  Unless of course you found it in the street tree inventory.

Thanks everyone! -- I'm the poster. I added some pictures of the bark and fruit earlier today but the edit did not go through. I don't care for the comment policies here so will be deleting my account.

That looks like a persimmon — your first image is of immature fruit.
Compare with:

UC Davis — Fruit and Nut Education
Google Image link

Good job... I was thinking about persimmon too, but for whatever reason could not find a picture of those leathery sepals.  Now I know.  The bark would have been distinctive.


text:
How protozoa spawns in newly formed ponds?
How big protozoa like Paramecium caudatum, Amoeba proteus, Euglena viridis etc. appear in newly created ponds of water? Suppose there was rain, and pond was formed. Or earth, dead leaves, live leaves and wood was added to bottle like in this video:
https://www.youtube.com/watch?v=j2T__l7FgU4
She says in this video that paramecium "should spawn from the dirt", but this makes no sense to me... Do they magically recombine from inorganic elements? Doubtful. Or maybe they are just scattered in every grain of dirt, everywhere, in a form of microbial cyst? Seems not very realistic either...
P.S. I'm mostly interested how Paramecium caudatum get in there, but if other protozoa have some other means, that would be interesting too.

Life does not generate spontaneously. Period.

Maybe the dirt include cysts and spores?


text:
Are chromosomal microdeletions passed on?
I've been looking around but can't find a clear answer: are chromosomal micro-deletions passed on (hereditary) or not?

Of course. Just like any other type of mutation.
If a mutation (incl. a chromosomal microdeletion) happens in the germ line, then the mutation can be passed on.

another question I may add/ask: if a parent has a chromosomal micro deletion, and uniparental disomy happens, then the child will inherit the deletion as well , right? Thanks for answering

Yes, necessarily. As both chromosome are passed (uniparental disomy), the one carrying the microdeletion will necessary be passed.

To be clear, microdeletion is the term for when a gene on one chromosome replaces its counterpart, yes?

@TheNate I think (but might be wrong) it is a term mainly used in the medical field. I think it refers to a small chromosome deletion (a few kb say) that is too small to be detected by the simple colouring methods (such as FISH or G-banding) often used in medicine.

Thanks. I'll go start some reading, then.


text:
Problem with Caspr antibody in western blotting
I have been working on optimizing western blotting for Caspr (contactin associated protein), but I am having difficulties and would like suggestions.

I ran my proteins on a 40% acrylamide gel,
I used TBST for washing and BSA as blocking buffer.
I incubated the blot with primary antibody overnight.
The secondary antibody is linked with HRP.

I could  not find any bands in the blot.(Same problem was faced in case of contactin) What might be the reason?
Edit:-

I repeated the experiment a couple of times and found that secondary antibody(Anti-mouse,1:5000)wasn't working anymore.
I made freshly diluted secondary antibody again and found bands.
The old secondary antibody dilution was only few months old.What may have gone wrong with it?

What percentage is your gel? And: Did you do Ponceau staining of the membrane?

The resolving gel was 8%. Yes, Ponceau staining was done.

And there you did see bands I assume. How old is your antibody dilution?

Do you have a positive control (actin or something)?

Usually you visualize the bands on the blot by exposing the blot to X-ray film or otherwise visualizing the HRP reaction, because you can't just see the reaction on the blot. Can you show us a film or other exposure of the blot? The blot itself looks ok but it's hard to say what the problem is without seeing such an exposure.

There were bands in ponceau staining. The antibodies are 2-3 months old.


text:
How can space travel affect women’s fertility?
From Time:

The reasoning behind the prerequisite, according to officials, is that
  spaceflight could potentially harm the women's fertility.

How can space travel affect a woman’s fertility?

The most obvious issue is exposure to radiation. Once you're beyond the earth's atmosphere and magnetic field you are exposed to much higher levels of radiation from cosmic rays and solar flares. It's also possible that microgravity (weightlessness) could have effects on the reproductive system, but this isn't well studied yet.
However, given the source you link to to (a nine year old article speculating on why China required female astronaut candidates to be wives and mothers), this may simply be a medical rationalization for a political decision. Radiation can damage male fertility too, and the effect of microgravity on the male reproductive system is also not well understood.

There's already too many men in China, compared to women (gotta love sex-selective abortion!), and I'd say cultural decision, not political.


text:
What physiological pathways lie behind inhalants hallucinogenic effect?
I searched through the web and surprisingly I found pretty much nothing on the physiology of hallucinogenic effects of inhalants. Any idea how people get high with inhalants (household and industrial chemicals) and what physiological pathway lies behind this mechanism?

Interesting question, although I'm not an expert on inhalants. But part of the many reasons of its psychoactivity may be of the less oxygen-saturated blood going to your brain (i.e. your body not having enough oxygen due to inhaling some gas).


text:
What is this seaside thing?
I found this on the sand and I do not know what is it? I thought it is sea devil, however I checked google and it is not. Can someone tell me what is it(its name )

Please include your location and the approximate size of the specimen. This will ensure you get the most accurate answer and will best make this post useful to others in the future. Thanks!

It looks like a worn-down water chestnut. Water chestnut fruits are often found along the shoreline and bottom of waterways - they have very sharp spines with barbs that can cause painful wounds when stepped on. Water chestnut is an aquatic invasive plant that is native to Eurasia and Africa. It was introduced in the United States in the mid-1800's as an ornamental plant. Around 1884, water chestnut was found growing in Collins Lake near Scotia, NY. Water chestnut colonizes areas of freshwater lakes and ponds and slow-moving streams and rivers and negatively impacts aquatic ecosystems and water recreation.
https://www.dec.ny.gov/animals/109536.html


text:
What’s the evolutionary benefit of cats playing with their prey?
I just saw a cat playing and teasing a wounded bird for minutes, and I immediately started to wonder what the evolutionary rationale were. After all, it seems eating the prey as soon as possible should be the optimal strategy (as you can’t lose what you have already eaten.).

The cat is probably just having fun. So, we could ask "What is the evolutionary benefit for having fun?" Through play, animal learn (Fagen 1974, Spinka et al. 2001, Pellegrini 2007, Hirsh-Pasek and Golinkoff, 2008). This is particularly true for juvenile. Adults play is not uncommon though and might follow from the same principles (Bekoff and Byers, 1998). Note that playing is also associated with reduced stress in adult cats (Bekoff and Byers, 1998).
Whether or not, the cat actually learn much through playing with its poor little prey (it probably learns to be a better hunter) is not really relevant. Playful behaviour, as a general behaviour may have been selected for. There would be no need for "playful behaviour with a pink string" to have actually ever been under selection. Many behaviours have evolved as side-effects of evolution of related behaviours.

If the cat doesn’t learn much by this “playfulness”, I imagine a strong negative selection would render this specific instance of risking resources a non-behavior very soon. And your answer begs the question, why a general “playfulness” trait would evolve, and what “playfulness” even is.

Why doesn’t a dog do this kind of behavior? I find dogs satisfy your very broad “through play, an animal learns” criterion. And the cat also doesn’t play with random stuff (you don’t see cats playing with sticks or fire or ...).

@HappyFace I imagine a strong negative selection would render this specific instance of risking resources [..] You have too selectionist a view of evolution. You might want to have a lookd at this post or maybe this post.

@Remi.b can you add some references and clarify the answer a bit? I mean, are you sure that this behaviour can indeed be described as "having fun"? Can it be something else (analysing the prey, for example)?  If so, can you also link some articles that say talk about positive effects of "having fun" (which sounds quite reasonable)?

@WYSIWYG I added some citations (and some texts as I learned by going through these papers)!


text:
What kind of bug is in this photo
Wondering what kind of bug this is found outside

I'm no expert, but it looks like a potato beetle to me: https://en.wikipedia.org/wiki/Colorado_potato_beetle Might be helpful to list location and other info to help people orient to what the possibilities could be.

Yes, it is robust like a Colorado potato beetle (Chrysomelidae), but its antennae give it away as a scarab.

That is a Ten-lined June Beetle, (Polyphylla decemlineata) in the family Scarabeidae. You can tell its a scarab by its lamellate antennae. The stripes indicate the species.
https://en.wikipedia.org/wiki/Ten-lined_June_beetle

Agreed as to genus; the species may be in error (we need a location to be sure); see here for a list of North American possibilities.

Yes, I may have been premature.


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

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


text:
How important is getting enough glucose for maximal brain performance / cognition?
I know from many studies that have been done, that resting versus active use of the brain has relatively similar overall energy expenditure levels.
On the other hand, however, we know that the brain along with our eyes require glucose in order to function properly. Ketone bodies, lactate, etcetera may act as glucose sparing agents, but certain parts can definitively only use glucose as an energy source.
Anecdotally, I’ve noticed that when performing low intensity mental tasks like jogging or hiking for example, if I haven’t eaten for a while and am in a fasted state, I might get hungry for a bit, but if I just keep on going, after a while I feel fine and can pretty much go on forever after that. With high intensity mental tasks like programming though, the feeling of hunger doesn’t really seem to go away, and if I try to push through it, it just results in consistent brain fog and an inability to perform at any meaningful level.
My theory is that in cases where high mental performance is not required, alternative sources of metabolism provide the needed energy to function, and where intensive cognition is required, the rate of glucose production is unable to keep up with demand from the parts of the brain that depend on it which effectively creates a bottleneck in the cognition process causing the aforementioned brain fog and low performance.
Is this what is actually happening though? I’d like to think that it makes sense, but I’d prefer to have a biologically accurate understanding first and foremost.

In short: skipping a meal lowers blood glucose levels, which can reduce cognitive performance, for example, memory.
Let's say that between meals you are in fasting state for 8 hours during which you do some desk work and some moderate exercise for 1.5 hours. With such level of physical activity, your last meal and your glycogen stores should provide enough glucose for all your body needs, including the brain. So, during this time, you do not need any ketones or lactate as additional source of energy. According to Medical Hypotheses, 2014:

Estimated amount of glycogen in the human organism is about 200–500 g,
  and in certain specific conditions could reach up to 1.0 kg, which
  seems to be optimal for human organism. This amount is definitely
  sufficient for keeping optimal concentration of glucose in the blood
  during usual fasting periods not exceeding 24 h (between meals, during
  sleep, in case of exercise, etc.)

Skipping a meal can lower your blood glucose levels. According to WebMD:

Normal blood sugar levels are less than 100 mg/dL after not eating
  (fasting) for at least eight hours. And they're less than 140 mg/dL
  two hours after eating.
During the day, levels tend to be at their lowest just before meals.
  For most people without diabetes, blood sugar levels before meals
  hover around 70 to 80 mg/dL. For some people, 60 is normal; for
  others, 90 is the norm.

Blood glucose fluctuations related to meals:

Image source: Wikipedia, Creative Commons License
In some studies (AJCN, 1998), skipping breakfast was associated with lower blood glucose levels and worse memory test but not intelligence test results:

This article compares the findings of three studies that explored the
  role of increased blood glucose in improving memory function for
  subjects who ate breakfast. An initial improvement in memory function
  for these subjects was found to correlate with blood glucose
  concentrations. In subsequent studies, morning fasting was found to
  adversely affect the ability to recall a word list and a story read
  aloud, as well as recall items while counting backwards. Failure to
  eat breakfast did not affect performance on an intelligence test.


text:
What kind melanin do fair or light skinned black or mixed people have, eumelanin of pheomelanin?
I am doing a study on melanin and conductivity but I cannot find the answer to this question anywhere. Do light complected black or biracial people have eumelanin or pheomelanin? or both?

Race is not a biological construct, which is why asking this question from a racial perspective is not productive. All major variants associated with pigmentation (including the production of eumelanin and pheomelanin) had evolved a very long time ago and were selected upon as humans migrated from Africa. People of African descent, being the most genetically diverse group of humans on the planet, vary greatly in pigmentation, because they represent that initial pool of variants https://science.sciencemag.org/content/358/6365/eaan8433

Pheomelanin is associated with paler skin, while eumelanin predomominates in people with darker skin — this is influenced by alleles of the MC1R gene Swope and Abdel-Malek, 2018, NIH article on MC1R.


text:
Why do people say that smallpox has been eradicated?
I keep reading things like “smallpox has been eradicated” or “there are only two samples of the virus left in existence in a lab somewhere”, but couldn’t there be a bunch of smallpox viruses in an alleyway where some infected person sneezed years ago? Is there some reason the virus can’t exist without a human host?

You may want to read this.

The viruses that caused smallpox (Variola major and Variola minor) are generally not stable in the environment (<24 hours as an aerosol), though they may persist for more than a decade within scabs Reviewed: Sinclair et. al., 2008 OSHA.
UV light is an excellent disinfectant, so typically any virus exposed to sunlight will lose rapidly infectiousness.
You may also find this answer to a related question of interest:
https://biology.stackexchange.com/a/59165/46609


text:
Is it unusual for populations of archaea to be found living inside trees?
The NPR News article and podcast Getting Fire From A Tree Without Burning The Wood begins with

A scientist walks up to a cottonwood tree, sticks a hollow tube in the middle and then takes a lighter and flicks it. A jet of flame shoots out from the tube.
It seems like a magician's trick. Turns out, there's methane trapped in certain cottonwood trees. Methane is the gas in natural gas. It's also a powerful greenhouse gas.

and describes the discovery that quantities of methane have been observed to be produced within cottonwood trees.
There is a video of the methane tapped from a tree being set on fire.
The article continues:
"The wood in this particular species naturally has this condition called wetwood, where it's saturated within the trunk of the tree," says the lighter-flicking scientist, Oak Ridge environmental microbiologist Christopher Schadt.

This wetwood makes for a welcoming home for all sorts of microorganisms.
"You can't actually see a lot of the organisms because we can't grow a lot of these organisms," says Melissa Cregger, a staff scientist at Oak Ridge. "So we're able to identify them using their gene sequences."
Some of those organisms turned out to be species of archaea that are known methane producers. So it's not the trees themselves that are making the methane, it's the microbes living in the trees.

It's not clear to me if the use of "wetwood" refers to the natural condition of cottonwood trees, or if this is meant to refer to some kind of bacterial infection. For example, Mirriam-Webster defines wetwood as:

wood having a water-soaked or translucent appearance because of abnormally high water content sometimes due to bacteria and sometimes to physiological factors

Question: Is it unusual for populations of archaea to be found living inside trees? Is this something new and surprising or is this well documented?

The exact term — wetwood, is used only once in the original article (Yip et al., 2018).

Others have found that water content of heartwood tissue was the best
predictor of methane flux across multiple plant species (Machacova et
al., 2016; Wang et al., 2017), however this was not a strong predictor
of methanogen relative abundance in our analyses. It is possible that
within trees characterized by wetwood such as Populus deltoides,
other factors may become more important than water content above a
certain moisture threshold.

However, if you look at these lines from the introduction of the paper, it seems that wetwood just means wood that has a high water content. It definitely does not refer to a disease or infection.

Indeed, both mechanisms may be important depending on tree species
(e.g. those containing dry and dense vs wet and porous wood) and
ecosystem under study (e.g. wetland vs upland forest soils).

Based upon past work and our own informal observations of odors
associated with tree coring at these sites indicative of fermentative
environments, we hypothesized that an anaerobic community including
methanogenic archaea would dominate woody tissue, particularly in
heartwood tissue which is often water‐soaked.

Now coming to your question on whether it is unusual for populations of archaea to be found living inside trees.
Roots have been known to harbour microbes; plants establish this symbiotic relationship with the microbes for nitrogen fixation (See mycorrhiza and root nodules). So, it may not be very unusual that archaea interact with plants but it may possibly be unusual that they are living inside this part of the tree. Yip et al. (2018) highlight that although microbial composition of the wood has been studied in the past, these studies have been done ex situ. This means they are the first to study these microbes in situ.

Microbiological investigations of living wood have been conducted in
the past (Zeikus & Ward, 1974; Zeikus & Henning, 1975; Ward & Zeikus,
1980; Schink et al., 1981a,b, 1982), but these studies primarily
focused on ex situ wood incubations and the isolation of microbial
representatives, rather than overall community characterization across
tree conditions. For example, Zeikus & Ward (1974) demonstrated that
methane production occurred from extracted wood tissue from Populus
deltoides and were able to isolate pure cultures of a new species,
Methanobacterium arborphilicum (Zeikus & Henning, 1975), later
reclassified as Methanobrevibacter arboriphilus (Balch et al., 1979).

So, it seems that people have been working on this area since 1970s.
However, it also appears that there is not much research on archaea as a part of the plant microbiome (Taffner et al., 2018).

IMPORTANCE: Archaea are still an underdetected and little-studied part
of the plant microbiome. We provide first and novel insights into
Archaea as a functional component of the plant microbiome obtained by
metagenomic analyses. Archaea were found to have the potential to
interact with plants by (i) plant growth promotion through auxin
biosynthesis, (ii) nutrient supply, and (iii) protection against
abiotic stress.

So whether this is unusual or not depends on whom you are asking (hence a bit opinion based).

This turns out to be more complicated than I expected, thank you for the interesting and well-sourced answer!


text:
What causes a tendinopathy to calcify?
I read in this 2012 research paper {1}:

The aetiopathogenesis of CT [calcific tendinopathy] is still controversial, but seems to be the result of an active cell-mediated process and a localized attempt of the tendon to compensate the original decreased stiffness.

Has the cause of calcific tendinopathy been more clearly determined since then?

References:

{1} Oliva, Francesco, Alessio Giai Via, and Nicola Maffulli. "Physiopathology of intratendinous calcific deposition." BMC medicine 10, no. 1 (2012): 95. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482552/ ; https://dx.doi.org/10.1186%2F1741-7015-10-95

The article that you linked states that the exact mechanism is not known but lists different theories. A question like "has anything more been discovered" is broad. Did you try checking the articles that cite this one? It's easy to do that on google scholar.

@WYSIWYG 109 articles cite this paper, and a paper that found the cause of calcification might not have cited this paper. I was hoping that some expert on this website already knows the answer. The question is clear and I don't think it is too broad: The question is "What causes a tendinopathy to calcify?" If that's too broad, you'll need more than 40 close votes per day.

The question "What causes a tendinopathy to calcify?" is broad indeed. There may be several processes involved at the subcellular and tissue level. It is not possible to list and explain every pathway involved. You must add more details to your question. You certainly know more than me about this field; you can look at more recent papers. The paper that you mention is the first hit on google. Since you study tendons you could definitely search more recent papers on this topic. You can add those findings and make your question more precise.

@WYSIWYG If the question "What causes a tendinopathy to calcify?" is closed as too broad, then a large portion of questions posted on https://biology.stackexchange.com should be closed for the same reason.

You can certainly vote to close them.

@WYSIWYG I don't think it's too broad, and I think one should cast close vote consistently across questions. https://biology.stackexchange.com/tour says "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students". The question  "What causes a tendinopathy to calcify?" is perfectly fine for student-level.

I don't want to go into an extended discussion but just to make you realize I'll throw a similar question at you: what causes diabetes? Tell me if it is broad or not. Anyway, I think your question is broad and needs more details and I am free to vote my opinion.

@WYSIWYG Not all "What causes X" questions are equally broad. In the example you gave, diabetes is a group of diseases and many factors play a role. The aetiopathogenesis of calcific tendinopathy is much more narrow in scope. I think that inconsistent close vote decisions are deleterious for the website, since it means that questions might be closed subjectively and not according to clear rules.

@FranckDernoncourt I agree with WYSIWYG. The problem is that if the answer is "Nope" it is impossible for someone to find a reference actually answering that. If the answer is "No, but X has found 1), Y has found 2), and Z has found 3)" since 2012, you've basically had someone write you a new review article; they should publish it instead of posting here. Only in the circumstance that there is a new canonical review that you are not aware of but exists as one of the 100 citations for that paper is there a sufficiently narrow answer for someone to post.

@BryanKrause "Only in the circumstance that there is a new canonical review that you are not aware [...] there a sufficiently narrow answer for someone to post" -> yes this is what I am looking for and this is why I wrote "Has the cause of calcific tendinopathy been more clearly determined since then?" in the question.

@FranckDernoncourt The best advice I ever got in grad school was from a senior grad student at the time passing on advice he got from his advisor. She cautioned him to study questions where the outcome is interesting no matter what, to avoid getting stuck in a place where you have an answer but it doesn't mean anything. Similarly, a SE question that is probably unanswerable is not a good question: it ends up either with a bad answer or it lingers as a bad unanswered question.

@BryanKrause Then your close vote reason is different from  WYSIWYG. If your reason is that "SE question that is probably unanswerable is", then 1) the study I mentioned is seven-year-old, science has progressed since then and there might be a clear answer by now 2) if experts in the field are aware that the question currently doesn't have any satisfying answer, then that's an answer in itself.

@FranckDernoncourt No, I think the reason is the same: either it requires a too-broad answer, or it is not answerable, therefore it is too broad. I think the probability of "Only in the circumstance..." is sufficiently low to ignore entirely.

@BryanKrause How do you view "not answerable" as "too broad"? One example of answer is "study X published in 2018 showed that aetiopathogenesis of  calcific tendinopathy is Y". Another example of answer is "study Z published in 2019 indicates that no consensus has been found so far" etc. The question is perfectly answerable.

@FranckDernoncourt I disagree and I've already explained why. I won't argue this further here.

@BryanKrause the question is perfectly answerable as my previous comment illustrates


text:
Species identification please - Bug is a plague for Italian Stone Pines (Pinus Pinea)
They hangout on the top of Pinus pinea and spray a sticky substance all over the place. Size is about 2mm (head and abdomen) may be 4mm including antennae and legs. Could you please help me identify it and understand some of its habits and biology? I took the photos in a coastal town in Southern Spain. Thanks!!

That's and aphid (Hemiptera:Sternorrycha). Most likely, it belongs to the genus Cinara, which is common on trees. https://en.wikipedia.org/wiki/Cinara


text:
What was the cause of some egg-laying animals evolution to animal-laying?
Is there a specific reason for this evolution? Are no egg-laying animals more complex beings so their embryonic  development requires more time and better nutrition conditions?

Oviparity to viviparity (and vice versa and middle ground with ovoviparity) has evolved a number of times. Is there a specific lineage you have in mind when asking this question?

Wikipedia > viviparity#evolution will probably give some useful information

No I think that first appeared oviparity an then viviparity.


text:
Explain to a layperson how cigarettes smoke might cause cancer
I have a very intelligent friend who is a light smoker, and also a Biology layperson.
I wondered whether understanding exactly how cigarettes smoke can cause cancer, might encourage him to smoke less (or quit entirely).
So how would you explain to a Biology layperson how cigarettes smoke might cause cancer?
To clarify, I am looking for a detailed explanation for a layperson, that makes the cause-and-effect much more vivid for them, and thus makes it much more likely that the intelligent layperson would internalize the risks of smoking.
Online resources that I found either gave a too simple answer or concentrated on statistics (which are usually hard for humans to internalize, if I understand correctly).
(Nothing wrong with such explanations, they are just not what I am looking for.)

I'm voting to close this question as off-topic because it is a request for proof-reading a document, rather than for an answer to a biological problem, which is what is appropriate to SE Biology. It might possibly be re-phrased as "How does smoking cause cancer?" with the bulk of the question being moved to an answer from the poster (which is allowed).

@David Is a solution for a biological problem in layman terms appropriate for biology.SE? anyway, I edited according to your suggestion (hopefully). Thanks :)

@David By the way, I wrote the question after I had already sent my friend my explanation (which wasn't even in English). I just thought that surely many biology.SE users could explain it better than me, and so I posted the question (which included my attempt at explaining it, as I thought that biology.SE requires showing your efforts in the question).

There are tons of resources on this, especially for laymen. Did you even try looking at them? Simple answer to your question is that cigarette smoke contains many harmful substances and some of them are carcinogens. Regarding your original question: you start with DNA replication and how a particular carcinogen can cause mutations in DNA. That is a very broad background and is actually counter-productive. In your current form, I might say that your question is broad and also not useful as there are loads of resources on this topic from reputed organizations, for laypersons.

@WYSIWYG I did some googling, but I admit probably not enough. I turned to biology.SE as I assumed that like this resource, most of the resources for laypersons don't get into detail, and aim at simple answers like yours. I probably didn't explain myself well: I am looking for a detailed explanation for a layperson, that makes the cause-and-effect much more vivid and thus makes it much more likely that the intelligent layperson would internalize the risks in smoking.

@OrenMilman If they go into details then laypersons won't understand. If one wants to understand how mutations happen in DNA then they have to look at other sources. Stackexchange format is definitely not suitable for answers like these: starting from DNA composition to the effect of carcinogens. There are too many processes involved and one can learn a lot about any of those processes. If you want to educate people then you can try writing a blog.

@WYSIWYG I posted at first because I thought my explanation isn't optimal, so if you think explaining DNA composition isn't relevant, I don't disagree :)  Anyway, I guess different SE sites are different, as I first got the idea to ask this from a stats.SE post.

In reply to your query whether an answer in layman's terms is appropriate for SE Biology, that is a matter of opinion. My opinion is only one of five needed to vote a question off-topic, and others may not agree with my reading of the rules. That said, it depends. On looking at your answer, I'd say that it probably isn't very useful here.

I encountered the following paragraph in the textbook Life: The Science of Biology:

Some chemicals add groups to the bases. For instance, benzopyrene, a component of cigarette smoke, adds a
  large chemical group to guanine, making it unavailable for base
  pairing. When DNA polymerase reaches such a modified guanine, it
  inserts any one of the four bases at random. Three-fourths of the time
  the inserted base is not cytosine, and a mutation results.

After finding the following quote in Wikipedia's Benzo(a)pyrene page, I decided to explain specifically how BaP can cause cancer:

BaP has since been identified as a prime carcinogen in cigarette
  smoke.

My explanation:

A protein molecule is a chain of amino acids. Proteins are hugely important, as they are responsible for most of the cellular functions.
A DNA molecule is a chain of nucleic acids. There are 4 types of nucleic acids in DNA: A,G,C,T.
Having intact DNA molecules is crucial, because they include the encoding of proteins, according to which cells synthesize proteins.
A mutation is an alteration of a DNA molecule.
A mutation might lead to our cells synthesizing a malfunctioning protein. If a protein that should regulate cell division is malfunctioning, then the result might be uncontrolled cell division - cancer.
When you smoke, the chemical BaP (which is found in cigarettes smoke) might alter a G nucleic acid in a DNA molecule in some cell in your body. Later, when this cell tries to divide, it makes a copy of each of its DNA molecules, but it won't be able to identify that G nucleic acid (that BaP altered), so it would put a random nucleic acid in the copied DNA molecule. Thus, there is a 3/4 chance for a mutation.


text:
How to tell the difference between mould and condensed milk and sugar
I have had sweetened condensed milk in the refrigerator for some weeks (or months perhaps?). The can was covered with aluminium foil.
I noticed some disk-like artefacts on its surface, which are harder then the rest of the product:

Full-sized photo
How can I know if this is mould or simply further condensed milk with sugar? Is this safe to eat?
If it is relevant: the content of sugar is 56 g per 100 g, while this product has 8 % of fat content.

You could try picking up a piece and putting on top of a slice of bread or some other nutrient in a sealable bag  and leave it on a counter overnight and see if it grows?

@Cell, that's a good idea, thanks!


text:
Is there anything that can tell me precisely how the cross sectional area/radius of a snake changes over length?
I am trying to 3D model a green anaconda which I thought would be simple, then I realized there is actually this very gradual change in thickness from a minimum around its neck to a maximum somewhere in the middle then to another minimum around its tail.
Is there some kind of specific terminology or archive I can look up to get precise measurements? Regular google searches aren't doing it and there is a high amount of variation in this thickness gradient between species.

Maybe just pick a function with such properties and adjust the parameters until the snake "looks right"?

@electronpusher that would work only if there is data. OP is asking for data, not modeling tips.

If there was a perfectly straight snake that had both top and side pictures of it next to a ruler, then I could take measurements until it "looked right", but unless I have at least that, there's no accurate way to approximate it other than shear guessing.