Deuteranopia confusion lines For people with protanopia (absence of "red" cones), confusion lines look like this (which is quite intuitive for me)

Analogous picture for tritanopia (absence of "blue" cones)

  But picture for deuteranopia is quite different. Confusion lines are
  intersecting at one point. But this is not a point nearby green color,
  it is opposite. Why?

I have a conjecture.
Let me remind you about RGB. There is a three-dimensional space (coordinates are RGB coordinates). There is a cone in this space which corresponds to all colors which we can possibly see. Then we consider a section of this cone by a plane. And this is your RGB diagram.

I think that people have chosen a random plane. There is a line for excitation of green cones only. And this the plane intersected negative part of the line. If we chose this plane more carefully, this the picture for green confusion lines would be similar to red and blue.

A friend of mine says that that choice of this plane is not random. It is a plane of constant brightness.
He even conjectured that "green" cone cells are activated not when they absorb green light, but when there is no green color at all.

  Is this plane indeed random?

For more details look up here

Is this plane indeed random?

Answer : I don't think so.

HUMAN CONE RESPONSE

Let's take a look back at human cone response curve.
This is cone response curve for normal people :

  But picture for deuteranopia is quite different. Confusion lines are intersecting at one point. But this is not a point nearby green color, it is opposite. Why?

In case for Deuteranopes, let's take a look at their cone response :

As you can see Deuteranopes have their green cone sensitivity shifted very close towards red.
This also why Protanopia and Deuteranopia is what we know as Red-Green color blindness, where they have difficulty in distinguishing shades of red from shades of green since its cones sensitivity is very close to each other (almost similar).

So for deuteranopia, why the intersecting point is it not green ? Well, despite the actual missing cone is green, its sensitivity is shifted towards red. Also, this "intersecting point" is called copunctal point.

CONFUSION LINE :

Now about confusion line, indeed each cones in our eyes is sensitive to each RGB primary (even though it's a little bit misleading). And yes, RGB color space is in 3-dimensional. But confusion line is mapped based on chromaticty diagram from CIE 1931, not RGB. Some specific transformation and normalization method need to be performed to convert 3-dimensional RGB into 2-dimensional chromaticity diagram.

As we know before, Protans and Deutans have their cone sensitivity close to each other, thus their copunctal point (point where the fundamental color is missing, point where all the lines converge) is also close to each other.

Here's the copunctal points (1) for all dichromats :

COPUNCTAL POINT     x         y
Protan             0.747     0.253
Deutan             1.080    -0.800
Tritan             0.171     0.000

CIE is quite tricky, they can have negative value as well (RGB can't have negative value). This copunctal point is very important since it's the fundamental information of the missing wavelength from colorblind, and this missing wavelength is converted into CIE colorspace and then mapped into the diagram. So, even though the deuteranopes confusion lines looks a bit confusing, it is the correct mapping from actual missing point in wavelength.

(1) Wyszecki & Stiles, Color Science (2nd ed.), 1982, Table 1 (5.14.2) p. 464


Are eukaroytic promoters located in the 5' UTR region? I was wondering if promoter sequences are located on 5'UTR region in eukaryotic organisms?

Most promoter elements are not a part of the mRNA sequence. They are upstream (towards 5') of the transcription start site. However, a certain class of promoters called downstream promoter elements (DPE) can overlap with the geneic region. These elements have been reported to lie at 29-33bp upstream of the transcription start site and widely employed, in Drosophila [1]. Mapping of DPEs has been done for mouse human genes as well [2]. However, a detailed analysis supported by good sequencing data is yet to be done.

So, though DPEs are present in the transcript, I am not sure if they are retained in the exon. This can be confirmed by mapping the splice sites but this analysis is not presented in these papers.

You can see from the below figure [3] that most first exons in humans are big enough to harbour the DPE.


What makes a rotator cuff tear symptomatic in humans? The majority of   rotator cuff tears  is asymptomatic {1}. What makes a rotator cuff tear symptomatic or asymptomatic in humans?

References:

{1} Minagawa, Hiroshi, Nobuyuki Yamamoto, Hidekazu Abe, Masashi Fukuda, Nobutoshi Seki, Kazuma Kikuchi, Hiroaki Kijima, and Eiji Itoi. "Prevalence of symptomatic and asymptomatic rotator cuff tears in the general population: from mass-screening in one village." Journal of orthopaedics 10, no. 1 (2013): 8-12. https://scholar.google.com/scholar?cluster=6848408356619886538&hl=en&as_sdt=0,22 ; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3768248/

  In conclusion, our survey of 664 residents in one village demonstrated that the prevalence of rotator cuff tear was 22.1% in the general population, which increased with age. Asymptomatic tear was twice as common as symptomatic tear.

  […]

  In this study, “asymptomatic” was defined as having neither pain nor
  any other symptoms related to the shoulder when the survey was
  conducted including the past history of shoulder pain, whereas
  “symptomatic” was defined as having pain or any other symptoms related
  to the shoulder when the survey was conducted.

  Caption: Prevalence of symptomatic and asymptomatic tears.
  Asymptomatic tear accounted for 50% of all tears in the 50s. However,
  in the 60s and over, the percentage of asymptomatic tear was
  significantly greater than that of symptomatic tear.

The underlying reason is difference in the rate of firing of torned and intact muscle in movement of shoulder joint.

Asymptomatic patients had minimal pain (<3 on the visual analog scale and no loss of active range of motion compared with the contralateral side); symptomatic patients had pain greater than 3 on the visual analog scale and decreased range of motion compared with the contralateral side (>10 degrees of motion loss). Electromyographic activity from 12 muscles and kinematic data were collected simultaneously during 10 functional tasks. Both symptomatic and asymptomatic cuff subjects demonstrated a trend toward increased muscle activation during all tasks compared with normal subjects. During the internal rotation tasks, asymptomatic patients had significantly greater (P<.05) subscapularis activity than symptomatic patients (65% maximal voluntary contraction [MVC] vs 42% MVC). During the carrying task, asymptomatic patients demonstrated significantly less (P<.03) upper trapezius muscle activation than symptomatic patients (16% MVC vs 50% MVC). During shoulder elevation tasks, symptomatic patients had significantly greater supraspinatus (52% MVC vs 28% MVC, P<.03), infraspinatus (32% MVC vs 16% MVC, P<.05), and upper trapezius (39% MVC vs 20% MVC, P<.04) muscle activation compared with asymptomatic patients. During heavy elevation (8 lb), asymptomatic patients showed a trend toward increased activation (P<.06) of the subscapularis compared with symptomatic patients (34% MVC vs 21% MVC). Differential shoulder muscle firing patterns in patients with rotator cuff pathology may play a role in the presence or absence of symptoms. Asymptomatic subjects demonstrated increased firing of the intact subscapularis, whereas symptomatic subjects continued to rely on torn rotator cuff tendons and periscapular muscle substitution, resulting in compromised function.

Source: Kelly, Bryan T., Riley J. Williams, Frank A. Cordasco, Sherry I. Backus, James C. Otis, Daniel E. Weiland, David W. Altchek, Edward V. Craig, Thomas L. Wickiewicz, and Russell F. Warren. "Differential patterns of muscle activation in patients with symptomatic and asymptomatic rotator cuff tears." Journal of shoulder and elbow surgery 14, no. 2 (2005): 165-171. https://www.ncbi.nlm.nih.gov/pubmed/15789010


If a human takes antibiotics are all bacteria in the body killed? From my basic understanding, antibiotics kill living things, bacteria for example.

Do the antibiotics consumed by a human-being distinguish between what they kill? Or do they just kill every bacteria they find? And if that's the case, which bacteria do antibiotics find or do they find all bacteria in a human's body? Again, if that is the case, does that mean that after taking antibiotics for a certain time that the human body is free of all bacteria?

No

There are several reasons why this might not be true, as Alexander has discussed. An antibiotic often has a molecular target that isn't present in all bacteria, it's extremely hard to get antibiotics to certain parts of your body, and some bacteria will be defended against a antibiotic attack by biofilms, resistance mechanisms, and sheer statistical probability.

That is not to say that many don't die. Indeed, one of the major causes of Clostridium difficile infection is that antibiotics kill most of your gut bacteria, allowing the somewhat better protected C. diff to proliferate, start producing toxins, and send you to the hospital with symptoms ranging from diarrhea to perforated colon and worse. That disease is a direct consequence of "Antibiotics kill some but not all bacteria in you".


How does a seed determine when to start germination? I'm sure there are many different ways for seeds of different species, but what is a general rule? Is it some kind of ideal temperature & wetness that triggers a chemical reaction? What factors stimulate seeds to germinate?

Certain conditions are necessary for seed germination:

Moisture — seeds dry out during dispersal, but at germination the cells need to absorb water in order to rehydrate so that metabolic reactions can take place, which will eventually lead to the growth of the embryo tops and shoot. Furthermore, some seeds contain a hormone that inhibits germination and water is needed in order to wash it out of the seed. The water needed for these processes is absorbed by the micropyle.
Warmth —  many of the metabolic events of germination use enzymes, and these are sensitive to temperatures. Temperature will often be used as a trigger for germination.
Oxygen — many of the metabolic events that occur during germination use energy. This energy is produced by aerobic respiration.

Many metabolic processes take place at the start of germination, such as the synthesis  of giberrellin, this is a plant hormone that stimulates mitosis and cell division in the embryo. Other plant hormones include Abscisic acid (ABA), which regulates seed dormancy and germination. It has been found to stop germination once it has been placed in the soil, it causes the seed to enter a period of dormancy. This allows the seed to remain dormant until when the conditions are more favorable for the seed to grow.


Why is glucose used in oral rehydration therapy? What is mechanism of action of glucose in the intestine to reduce the watery and electrolyte secretion?

Oral Rehydration Therapy uses electrolyte solution containing some glucose. It is because, the absorption of electrolytes is more efficient when glucose is added. Sodium uptake from intestine is carried out by sodium glucose co-transporters.


How do you check how many cones you have in your eye? Following my previous question: What color does the other cone in Tetrachromacy correspond to?

People with normal color vision posses 3 cones in their eye. But there are some rare cases when people can have 4 cones (Tetrachromacy). These people, some of them will notice the shades difference in the scene through their eye. And the rest won't notice it, because simply their 4th cone is activated in the close peak value with the the L-cone. Therefore eye will not find any difference and will encode only one color even if it's coming from 2 cones stimuli.

How do you check, to know how many cones you have in your eye ? If the case is, even people who posses 4 cones can't even notice the shades difference ?

One of the two confirmed cases of tetrachromacy was confirmed genetically:

From this Popular Science article:

  Based on Antico's genes, Jameson has determined that Antico's fourth
  cone absorbs wavelengths that are "reddish-orangey-yellow, but what it
  appears to Concetta is uncertain at the moment," she added. Since the
  tests aren't calibrated for this wavelength, empirically demonstrating
  tetrachromacy is still really difficult.

Color vision is connected to the X chromosome and mutations in the X chromosome cause less or more color vision.  In the above case, the theory that people with 2 mutated X chromosomes could have four cones instead of three was tested.

This image from Scitable by Nature Education articles simulates regular vision on the left and tetrachromatic vision on the right:

As far as how to test to see how many cones you have, there are some online test that may or may not be very reliable.  This Metro news article has a test produced by Professor Diana Derval, author of "DesigningLuxuryBrands: The Science of Pleasing Customers’ Senses.  However, due to the limitations of computer screens it would not be reliable to test for tetrachromacy.


Why is therapeutic index a ratio instead of an interval? The therapeutic index of a drug is defined as its toxic dose ($TD_{50}$) divided by its effective dose ($ED_{50}$).  Why is it defined as a ratio rather than the difference $TD_{50} - ED_{50}$?

For example, if drug A has an effective dose of 1 ml and a toxic dose of 2 ml, and drug B has an effective dose of 50 ml and a toxic dose of 100 ml, then they both have the same therapeutic index (2), but intuitively, I would say drug A is much more dangerous, which is reflected if we take the difference instead.

Most drugs are measured by mass - they are then dissolved in some solution or incorporated with fillers into pill form.

If you are worried only about a difference, say from measuring out a volume to be given intravenously, then it would be trivial to solve that issue by dilution: you could take your drug that was dissolved in 1 mL, dilute it so that you are giving 50 mL instead, and make the difference unimportant. The ratio, however, stays the same, regardless of formulation.

A ratio is also much more likely to come up in clinical practice. Take your example, where the toxic dose is only 2X the effective dose. That means that an error where a drug is accidentally given twice could be a serious problem. It doesn't really matter if the volume delivered is small or large, just that someone doesn't realize the drug was already given.


How many senses do humans have? I recall learning that humans have 5 senses, but that may have been an over-simplification to focus on the most notable ones, or simply that no others were known about at the time. Wikipedia says:

Although traditionally around five human senses were known (namely sight, smell, touch, taste, and hearing), it is now recognized that there are many more.

Is there a known, discrete number of senses (and, if so, how many are there)?
Note: If there's disagreement in the scientific community about the answer it would be interesting to learn what most biologists consider most plausible.

I'd like to challenge your question.
What is a sense?
Are you looking for a complex organ that integrates with the central nervous system? Or just any part of your body that can be used to determine the property of something in the outside world? For example, you can use your toenails to test whether a hot plate is of sufficient temperature to melt dead keratinous biomaterial, like your nails. This would count as an integrated sense for a specific physical chemistry.
Or do you think a sense is a thing that detects a singular property of the world? For example, do you discriminate proprioception from gravity sensing, even though it may be performed by the same organ? Historically, each classic sense is limited to one property, but this I think is outdated. For example, skin is not only capable of performing touch and texture detecting ("tactile" sense), but also heat, pain, and other things like sensing noxious poisons such as bee stings.
Also, do senses have to detect stimuli in the external world? Plenty of sensing goes on internally, both in interstitial spaces and fluids in your body, on the surface of cells, as well as within cells, and the variety of cellular and sub-cellular equipment is hugely various. Should light receptive cells only count as 'vision' or 'light receptive' when they are found in the eye, or can light-sensitive cells found deep within the body can also be classified as part of the visual sense? There are many animals and tissues in biology where light-sensitive receptors are not exclusively found in eyes.
These are only 3 things you did not consider. There are many other questions you must answer along these lines to have a clear, at least temporarily operational definition that can be used to make distinctions to answer what things can count as a separate, countable sense.
Just as a proof of concept, I can list more than five senses off the top of my head to show you that the "five senses" concept is woefully outdated in my view, and I'm sure some others would agree. I will pick some weird examples just to demonstrate the complications that the above questions illustrate.
Chemosensory systems
(considered a sense for chemistry? or a collection of senses?)

Olfaction (smell, as carried out by neurons in the nasal epithelium; e.g. smell of vanilla, and smell of bad food)
Gustation (taste, as carried out by neurons on the tongue; e.g. salt, sugar)
Antigen chemosensing (chemical sensing, as carried out by, for instance, immune antigen receptors on B cells)
Hormonal signaling chemosensing (chemical sensing of hormones such as insulin, as carried out for instance by myocytes)
Starch sensing? (amylase in saliva can be used as a test for digestable starch)

Visual system, at the retina?

Visible light (sensing electromagnetic radiation on the order of a few hundred nanometers in wavelength)
Internal methanol sensing (the visual system as a sensor for methanol, which disproportionately affects myelin surrounding the optic nerve)
Pressure sensing (see phosphenes)

The vestibular system

Gravity sensing
Balance
Coordination
Motion sensor
Head position sensor
Spatial orientation

Skin

thermosensation (touching a hot kettle!)
Nociception (pain sensing)
allergen sensing
sensor for gamma rays, X-rays and UV light (indicated by radiation burns, development of skin cancer, sunburns, etc.)

Bones and muscles?

Kinesthetic and bodily proprioception

Brain/mind/mental/social senses?

mental pain
boredom
mental or spiritual distress
sense of self and other, including friendship, power, place in social hierarchy, reputation, companionship
motivation and love (oxytocin, dopamine, etc. in limbic systems and other neural correlates)

I'm sure some would agree, and some would disagree about the specific cases I provide. Thus the definition of senses, or sensing, seems to be opinion-based or at the very least very sensitive to an agreed-upon operational definition, for which there is none.


Does pepsin digest plant protein? This may sound trivial, but...

Protein is sourced from plants and animals. Pepsin and HCl digest meat (animal protein). Does pepsin also digest plant-based proteins?

I took a look at few articles online and this. None seems to explain what I am after.

Yes, pepsin does digest plant proteins also. Pepsin is a protein and its job is to cut other proteins (also known as polypeptides) into smaller pieces. Proteins are made of amino acids and there are 20 amino acids found in proteins. Pepsin cuts the bond between two amino acids to break the protein into smaller pieces. When pepsin encounters a tryptophan (Trp), tyrosine (Tyr), and/or phenylalanine (Phe), it cuts the bond between that amino acid and the one next one, as shown below.

image source

Proteins from plants contain these amino acids so pepsin can cleave plant proteins.


Wounded Pigeon in my balcony There is a, probably wounded, pigeon (common rock pigeon) in my balcony. It is dark right now and thus, I have very little idea about its condition. But it seems it is finding it difficult to fly/move its wings because when I approached the balcony door, it 'walked' towards the farther end of the balcony while flapping its wings very slowly.
What is the right way to handle the bird and what is the best thing I can do for him/her?

If you have a cat carrier then trying to intice it inside with some food would be a good idea. Try to contact your local wildlife vet for information on whether they would be willing to treat the animal. If you think it may be injured then I wouldn't reccomened handling the bird as you may hurt it further, but if you do need to then handle it by placing both hands over the wings in order to pick it up (https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/if-you-find-an-injured-bird/) . In addition the bird could have gotten used to its injury and learned to live with it so you could monitor it for a bit and see how it's getting on. Hope it turns out alright.
If you live in the UK here is some advice from the RSPB: https://www.rspb.org.uk/birds-and-wildlife/advice/how-you-can-help-birds/injured-and-baby-birds/sick-and-injured-birds-faqs/#:~:text=For%20most%20injured%20birds%2C%20place,how%20you%20can%20help%20it.


(how) is it possible to choose the biological sex of a child? I recently read of a study that investigated the ethics of child's biological sex choice in humans, and now I want to find out how this can/could be done. Does anyone know of scientific papers or journals that describe the methods in some detail? The answers I was finding in my own search were not as specific as I would like.

The main technique is sperm separation or sorting, where you separate sperm by gender, and only use the gender that you want. Existing techniques aren't perfect. AFAIK, they are typically less than 90% accurate, but it is still better than 50%. Typically, this involves some type of cell sorting device often with some kind of fluorescent tag marker.

The second technique is embryo screening. Often, with IVF, you screen and can confirm the gender that you want before implanting the embryo in the mother.

Links:

http://www.fertility-docs.com/programs-and-services/gender-selection/select-the-gender-of-your-baby-using-pgd.php

http://www.in-gender.com/Gender-Selection/MicroSort/


How are the correct tRNAs transported to the ribosome? I have been trying to understand how the tRNA transporting the correct amino acid required by the ribosome reaches the ribosome. The only way I can imagine this happening is that all types of tRNA+amino acid reach the ribosome, bombard the ribosome, and the ribosome will 'accept' only the one that matches what it is waiting for.

I can not imagine any other mechanism in the cell's cytoplasm that will somehow filter or push the correct tRNA+amino acid and move it towards the ribosome that needs it.

How do we explain this mystery?

The only way I can imagine this happening is that all types of tRNA+amino acid reach the ribosome, bombarding the ribosome, and the ribosome will 'accept' only the one that matches what it is waiting for.

Yup, basically.  This is an extremely cool figure showing the process. There are various elongation factors that aid the process, such as EF-Tu, which essentially waits until there is a good codon-anticodon match before hydrolyzing GTP and allowing the tRNA/amino acid to enter the ribosome.

This process can be particularly salient when you look at a concept such as codon-usage bias.  Certain tRNAs are more common in the cell, so if a given mRNA uses codons to match those tRNA instead of matching other degenerate but less common anti-codons, translation will occur faster.  This is more obvious in organisms such as E. coli where growth is paramount.


Why can I see a light flicker when it's in my peripheral vision? When I'm looking at an old CRT monitor or a worn fluorescent lamp, but not directly in the center of my gaze, the light from it seems to flicker. When I focus my gaze onto the monitor or lamp, the flickering stops.

Why can I see a light flicker only when it's in my peripheral vision?

Your retina contains both rods and cones. Cones are color sensitive, slow, and concentrated near the center of your field of vision. Rods are "light" sensitive, fast, and concentrated near the periphery. You want to be able to respond quickly to a threat "in the corner of your eye" without needing to see the color of the threat.

This is nicely explained by this diagram (source: http://hyperphysics.phy-astr.gsu.edu/hbase/vision/imgvis/retina.gif)

So when you see a CRT in the corner of your eye, your rods respond quickly enough that you can tell the light of the CRT is flickering. As you turn your gaze towards it, you get the higher resolution, color rendition of the cones - and lose the temporal resolution.


Does "Garbage Enzyme cleaner" contain cleaning enzymes? There are many recipes which call for using fruit peel fermentation process to make a concentrated enzyme cleaner solution, some variations call to add bakers yeast. So the question arises that does this recipe really have those cleaning  enzymes and how are they generated?

This says that it may not have the cleaning enzymes, but maybe some other cleaning agents like vinegar or alcohol.

A discussion from two independent researchers on this topic give contrasting positions

Moreover if fruits  like Pineapple and papaya are used does it make the solution more potent?

The discussion you linked (here) shows that both researchers agree that 'garbage enzymes' are mostly acetic acid or vinegar, with a low pH(3-4). Fresh papayas contain papain, but roughly 2% of the enzyme self-digests per day in aqueous solution. Bromelain from pineapples is still active at acidic pH. Like most other proteases, it self-digests much more rapidly than papain. As a result, any digestive enzymes present when the mixture was made would destroy themselves by the time the mixture matured.

((Those among you quick at math will note that perhaps 1/5 of the papain activity would remain after ninety days. While true, there's evidence yeast cultures eat gluten for sustenance, and if they can digest gluten they'll digest papain. There's no reason to expect yeast to leave a delicious protein source unused.))

If the solution acquired proteases somehow, they would self-digest under the conditions the 'garbage enzyme' solution is stored at(room temperature, aqueous solution, nothing exotic like formaldehyde, months). The yeast itself by the time the fermentation is complete has died, destroyed by the acetic acid(or ethanol, depending) they created. Any digestive enzymes used by the yeast to dissolve proteins destroy themselves as the mixture matures and the yeast die off.

If the mixture starts with no digestive enzymes, there's no mechanism to get appreciable amounts active digestive enzymes. If the mixture does start with digestive enzymes(papaya or pineapple), either the yeast will eat them and then die or they will digest themselves and the yeast will eat the byproducts. Finally, the yeast will die.

It's a vinegar/alcohol blend, depending on how much oxygen is available during the fermentation, and it smells like whatever you put in it. If you used orange peels, it probably smells pretty okay. That's why it cleans.

If you are anxious to use real live proteases, there are powdered papaya/pineapple/etc powders you could reconstitute in water right before use. They are usually sold as meat tenderizer among other things. There are also blends of enzymes sold for pet urine deodorizing, and general purpose cleaning fluid with bacterial and enzymatic action. Formulating those at home is going to be fairly involved, but if you wanted an enzymatic cleaner you made yourself that's how to do it.


Restriction Mapping of Plasmid Assignment pUWL22 is a circular, double stranded, 10.5 kb plasmid. It contains a
  gene encoding an enzyme that confers ampicillin resistance in the host
  bacterium. Cloning into the kpn I and Sst I sites abolishes ampicillin
  resistance, whereas cloning into other sites on the plasmid does not.
  Digestion with the following restriction enzymes singly and
  combination results in the following data:

Enzyme Digest     ()()()()()()   Fragments Produced (kb)

Hind III  ___________________________10.5

Kpn I  _______________________________10.5

Not I  _______________________________10.5

Pvu II  ______________________________10.5

Sst I  _______________________________10.5

Stu I  _______________________________10.5

Hind III + Kpn II  ___________________8.5  _______________2.0

Hind III + Not I _________________8.0  __________________2.5

Hind III + Pvu II ________________6.0  __________________4.5

Hind III + Sst I _________________7.5  __________________3.0

Hind III + Stu I _________________7.5  __________________3.0

Stu I + Not I  ____________________10.0  __________________0.5

Stu I + Pvu II  ____________________7.5  __________________3.0

Now the actual questions:

  A) Create a circular map of pUWL22, designating the Hind III site as
  the position 0 on the map. Once you have completed the map, indicate
  the relative position of the ampicillin gene.

My plasmid mapping:

What I need help with in indicating the relative position of the ampicillin gene. In the statement above it said "Cloning into the Kpn I and Sst I sites abolishes ampicillin resistance." Does that mean its inbetween Sst 7.5 and Kpn 8.5? Please tell me where it is and why its there.

P.S. I made a mistake on the on the Sst I enzyme, it's suppose to be @ 7.5 not 7.8.

The question after that is:

  B) Propose 2 other double digests that could be done to confirm your
  analysis. Predict the sizes of the fragments that would be generated
  from these digests.

Please answer this and explain why.

A) Here is the correct map:

You made a mistake on your map at the PvuII site (it is not on 6.5kB from the start of the plasmid, but on 6kB).

  Can the Kpn I not go on the 8.5 site, it still creates the 2 and 8.5, so isn't there more than 1 correct option for plasmid map?

Yes. What you need to do in order to make the correct map is try all possible positions of the restriction sites:

You start with HindIII and place it at position 0 of your vector.
The KpnII site can be either at 2kb (left of HindIII) or at 8.5kb (right of HindIII). Draw both versions of the plasmid.
You place the NotI site that can either be at 2.5kb or at 8kb. Now you have four different possibilities for the plasmid:

HindIII[0], KpnII2, NotI[2.5]
HindIII[0], KpnII[8.5], NotI[2.5]
HindIII[0], KpnII2, NotI[8]
HindII[0], KpnII[8.5], NotI[8]

Then you do the same for the rest of the restriction sites. When you get to the last two digests, there is only one option for the correct plasmid left in the following order, depicted on the plasmid map below.

I have to point out though that StuI and SstI can both be at 3kb (they can be next to each other). Then the 2 fragments from the digest will be ~3kB and ~7.5kB. So technically, there are two possible versions:
correct

a) HindIII[0], KpnII2, NotI[2.5], StuI[3], PvuII[6], SstI[7.5]

b) HindIII[0], KpnII2, NotI[2.5], StuI[3], SstI[3] PvuII[6]

  If u can, can u please elaborate on question b as to why there is one correct option for the plasmid map? Also, what do they mean by double digest to confirm ur analysis?

A double digest means that you cut your plasmid with two different restriction enzymes at the same time. As you already have a putative map of the plasmid, you can predict which would be the expected bands. If you observe the expected sizes, then your design is correct and your analysis are confirmed.

To check which one is correct I would do a double digest with:
1) SstI and PvuII, generating a 1.5kb and a 9kb bands if design a) is correct or                              3kb and a 7.5kb bands if design b) is correct
2) StuI and SstI, generating a 4.5kb and a 6kb bands if design a) is correct or                             a 10.5kB band if design b) is correct

  To confirm the "ampicillin gene" starts at kpn I 2.0 and end at the 3.0 stu I site right?? So the amp gene is 1 kB long?? So the relative position of the amp gene starts at 2.0 and ends at 3.0.
  Why is it that in the question it says cloning into the kpn I and sst I sites abolishes ampicillin resistance whereas cloning on other sites does not?
  What do they mean by this? Is the ampicillin resistance gene diff from the ampicillin gene??

The ampicillin resistance gene and the ampicillin gene are the same. It refers to an enzyme (beta lactamase) which degrades ampicillin, and thus the cells that harbour the ampicillin-containing plasmid can survive when plated on ampicillin.

Are you sure that the resistance is disrupted if cloning into SstI site and not StuI? If this is really the case, then the StuI site and SstI sites are next to each other, as first you have the SstI site, followed by StuI. The amp gene
The gene is a little above 1kb, so it starts upstream of KpnII and ends right after SstI, but it doesn't disrupt StuI. If something is cloned into KpnII or SstI sites, then the open reading frame of amp is disrupted, and the protein cannot be functional.


When does oxidation destroy prions? It seems like a no-brainer than oxidation, playing the, er, role it does in the universe, would destroy prions just like it destroys everything else.

But when does it do that? I assume this has been studied, since people handle them in laboratories and may need to sterilize their instruments.

Prions are fairly resistant to traditional method of sterilization.

Citing from: Guideline for Disinfection and Sterilization of Prion-Contaminated Medical Instruments

  The prions that cause CJD and other TSEs exhibit an unusual resistance to conventional chemical and physical decontamination methods. Because the CJD agent is not readily inactivated by means of conventional disinfection and sterilization procedures and because of the invariably fatal outcome of CJD, the procedures for disinfection and sterilization of the CJD prion have been both cautious and controversial for many years.

The same paper also lists several effective and ineffective methods for sterilization (efficient method have > 3log10 reduction in prion content within 1 hour)
I am not going to list them all here but you can see Table 2 in the paper.

Just to answer your specific question about oxydation, certain oxydising agents are effective, others are not. Similarly certain autoclaving (=sterilising with heat) procedures are fine and others are not.

Another interesting paper Methods to Minimize the Risks of Creutzfeldt-Jakob Disease Transmission by Surgical Procedures: Where to Set the Standard?


What are senescent cells doing in our bodies? I'm reading a paper that mentioned the elimination of senescent cells delays aging. I'd like to receive more information about it.

The Baker study published in Nature demonstrates that targeted elimination of senescent cells in mice results in remarkable protection from several age-related pathologies, cancer, and makes cancer cells resistant to chemotherapy. I know that senescent cells drive aging, and induce cancer. Can we grow them in cell culture as a kind of stem cells ? How might they contribute to the aging process ?

Senescent cells are cells that go into permanent cell cycle arrest. Although they may be metabolically active, they are not actively dividing. This may occur when cells in our bodies undergo damage from an extraneous or endogenous source. I understand that its role in cancer and aging is a great topic of study.


What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top) What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)

The insect in the picture was slightly damaged after an altercation with a human.

This is a cockroach.

Although about 30 species typically associate with humans and human habitats [source], the only ones that I know that have strong parallel dark lines running in the rostral/caudal direction are the Asian cockroach (Blattella asahinai) and the German cockroach (Blattella germanica).

According to Wikipedia, these 2 species appear very similar. At the adult level, it's actually more behavior (B. asahinai is a better flyer and tends to fly toward light) and habitat (B. asahinai prefers living outdoors while B. germanica prefers living indoors) that "best" differentiates these two species.

Your specimen is not an adult, however, as is made very clear by the extension of the dorsal parallel stripes extending beyond the pronotom, by the relatively small size of your specimen (<10 mm long), and by the absence of clearly-developed wings [see here for descriptions].

This wingless and long-striped specimen is an immature nymph. Although UFL indicates that late instar roaches of these two species can be identified by the presence of white spots on the dorsal abdomen of the Asian roach, your specimen appears to be an earlier instar and does not yet have this spotted pattern.

As in the adult stage, the early instars of B. asahinai and B. germanica also appear quite similar:

 German (left) and Asian (right) early instar nymphs. Photograph by Dina L. Richman (University of Florida); [source].

German nymphs are slightly smaller than Asian roach nymphs, but again they are quite hard to tell apart (often times being less distinct that the above picture).

I've been told that the most useful way for differentiating is simply by location: if found indoors it's more likely German and if found outdoors it's more likely Asian.

Regardless, if it was found inside, you need to act quickly to prevent an infestation...


What is the difference between intracardiac and extracardiac reflexes in cardiac regulation? The primary parameters of heart pumping are

strength of contractility (inotropic positive; Frank-Starling relationship)
rate of relaxation (lusitropic positive)
heart rate (chronotropic positive)

which change the secondary parameters according to the marginals

Heart rate
Stroke volume

Contractility
Starling relationship

Which of these paramecers are controlled intracardiacally and which extracardiacally?

Rate is controlled outside the heart by the Vagus Nerve having parasympathetic activity on the sinoatrial nerve.

Stroke volume (taking contractility and Starling's law as one) are factors from the cardiac tissue itself - "intracardiac".


How can rhodobacter possess a single 'PS-II' like reaction center? I recently came across an information in my book Trueman's Elementary Biology ,  a popular text in India, that photosynthetic bacteria like Rhodobacter, Rhodopseudomonas etc. possess a single photosystem where the reaction center is PS-II like. Now how can PS-II work as a single unit? As far as I know, PS-I can operate singly in cyclic mode generating ATP only. But PS-II works in conjunction with PS-I to generate ATP, $\ce{O2} $ and $\ce{NADPH} + \ce{H^+} $. So how can PS-II work as a single unit in this case?

McEwan (1994) Photosynthetic electron transport and anaerobic metabolism in purple non-sulfur phototrophic bacteria. Antonie Van Leeuwenhoek 66: 151-164.

...The purple non-sulfur bacteria ... carry out photosynthesis under anaerobic conditions. Photosynthetic electron transport is cyclic and involves ... two redox complexes ... reaction center (RC) [and] cytochrome bc1 complex. ... This cycle of electron transfer, [mediated
by ubiquinone (UQ) and a c-type cytochrome,] is linked to the generation of a proton motive force ... across the cytoplasmic membrane.


How do the quantities of ATP formed during aerobic and anaerobic respiration compare? How do the quantities of ATP formed during aerobic and anaerobic respiration compare?

You means fermentation and respiration?
In aerobic,1 mol glucose trough respiration and get about 38 ATP
In anaerobic, 1 mol glucose through fermentaion and get 2 ATP


Why do pandas have a high probability of giving birth to twins? According to the BBC documentary "Wild About Pandas", about half of panda birth result in twins.  Why do they have such a high probability compared to other mammals?  What factor(s) control that fraction in general for mammals?

Additional question about the allometry formula:

I am a little surprised that it is not the ratio between the neonatal mass and the adult body mass that enters the formula, but just the neonatal mass.  Any ideas on that?

Charnov and Ernest (2006) present data on offspring number per year and neonatal mass for 532 species of mammals. The two are related by the linear regression equation:

ln(offspring/year) = 2.4 - ( 0.3 * ln(neonate mass) )

Giant panda neonates weigh 100-200 g and are weaned at 46 weeks.

So, according to the regression, pandas should have, on average, 2.8 to 2.2 offspring per year (for 100 and 200 g respectively). With a weaning time of 46 weeks, they could have 1.13 (52/46) litters per year. If every litter were exactly twins, that would be 1.13 * 2 = 2.26 offspring per year, which is within the predicted range.

Humans (neonatal mass of 3400 g) are predicted to have 0.96 offspring/year.

Charnov EL and SKM Ernest. 2006. The Offspring‐Size/Clutch‐Size Trade‐Off in Mammals. American Naturalist 167:578-582.


Species richness corrected for area -- should area be log-transformed? I am doing a study to compare plant species richness (total number of species per site) to a bunch of environmental factors of sites at which these plants were surveyed. Because these sites are different in size, I have converted species richness to a species density measurement by dividing by the log of site area (species density = species richness/log[area]).

I log-transformed area, because the relationship between species richness and area at my sites is linear on a semi-log scale. Now that I have calculated species density in this way, I am having a hard time convincing myself that calculating density with log(area) was the correct approach. Does anyone have some insight on this? My community ecology background is not strong and I am getting bogged down in the literature.

Thanks!

Let me offer my answer even though I have not worked in ecology.

You are asking two questions if I understand you correctly:

Should you normalize to the area sampled?

The answer to that depends on whether the area sampled is a nuisance variable or not. Is it the case that you just happened to sample from areas with (largely) different sizes? Or do you rather expect or are interested in whether it may display some interaction with the environmental factors that you study? In the first case, normalize with clear conscience. On the latter, you should probably include the area sampled in your model. The reason for this is that by normalizing, you are assuming that the relationship between the response variable (number of species) and the predictor (area sampled) is fixed and has a slope of 1 irrespective of the variation of the rest of the variables included in your model. If that is not the case, you want to explicitly add the area sampled as a fixed factor in your model.

Should you log-transform the area sampled?

If the answer to the first question is that the area sampled is a nuisance variable then it does not matter whether you log-transform or not as now you are interested in a new measurement, species density. Hence, you may work with the untransformed variable which would simplify the interpretation of the results by a tiny bit. If the answer to the first question is that you want to investigate the interaction of the variable 'area sampled' with your other predictor variables, then you do not need to log-transform your variable as this is rarely needed, even if you use parametric inference. To summarize, you do not need to transform the variable 'area sampled'.


How can sex ratios remain Fisherian (1:1) in species where only the dominant male gets to mate In certain species only the dominant male gets to mate (or given strong preference), and yet the sex ratio remains 1:1. (I'm thinking in particular of gorillas). How does this happen? It doesn't seem like Fisher's argument should apply in this case.

Fisher's principle applies to such cases as much as it does to species where only pairs mate.  Consider a species where a successful male has exclusive mating with a harem of 20 females, and for each such male, 19 other males are not able to mate.  A female has 100% chance of mating, and a male has a 5% (1 in 20) chance of mating. Assume a female has two offspring.

In this scenario, an equal sex ratio would mean having a female offspring would lead to an expected number of grand-offspring of 2 (100% chance of 2 offspring from that female).  Having a male offspring would also lead to an expected number of 2 grand-offspring (95% times 0 offspring plus 5% times 20 harem females each having 2 offspring).

What would happen if the ratio of births was off from 1 to 1, say 5 females were born for each male? Then expected number of grand offspring would be for a female is still 2, but for a male it is 25% (chance of taking a harem of 20 females against the 3 other males born alongside those 20 females) x 40 (20 harem matings x 2 offspring) = 10. Hence with a lopsided sex ratio in this situation, having a male is much more valuable genetically than having a female.  If a mutant arose which produced more male offspring in this imbalanced situation, it would have success until the population sex ratio became close to 1:1.


Does any molecule other than DNA have a double-helical structure? DNA is known to have a double-helical structure. Do any other molecules have this structure?

A few examples:

Starch
A polymer of glucose that can form a double helix and functions primarily as energy storage in plants.

[image source]

f-Actin
Filamentous actin forms a helical structure with two strands of polymerized g-actin. This is a structural component of the cytoskeleton.

[image source]

Coiled Coil
Protein motif with a helical structure formed by two (or more) α-helices. Coiled coils are found in a diverse range of proteins from structural proteins like keratin to transcription factors like c-Fos.

[image source]

Gramicidin
A peptide-based antibiotic that has been shown to form membrane spanning double helices.

[image source]


How can a three-base codon evolve from a two-base codon? Inspired by this question among others.

It's widely suggested that the current 3-base codon system of encoding protein sequences in DNA evolved from an earlier 2-base codon system. This makes sense if you look at the coding sequences themselves but I fail to understand how it can evolve? Wouldn't any shift wreck the coding of all existing proteins?

Perhaps they could overlap, but wouldn't even that produce nonsense and how would it shift to non-overlapping codons? Perhaps both systems could run in parallel, but how would anything useful come from that in the short term? What selective of advantage of 3-base coding could be strong enough to overcome any disruption?

Has anyone developed a coherent model of what intermediate stages might look like?

It is not suggesting a 2-base->3-base code in the way you are thinking, but of a non-coding, two-coding triplet pattern occurring first.

This means you would have 16 different coding sequences with 4 possible spacing bases in between.

Later, the spacing bases could become used as part of the code.

Does that make more sense?
Instead of AA,CG becoming AAT,CGT; AAX,CGX becomes AAT,CGT etc.

Its also likely that between 2 and 3 base codes a 2 base pyrimidine/purine system was used. Today the third base can often be switched for its pyrimidine/purine pair without changing the resulting amino acid.


Microorganisms in Louis Pasteur's experiment of beans Louis Pasteur's experiment proves that microorganisms do not grow from non-living matter, he discovered that microbes can cause food spoilage.
So, where do microorganisms come from? Do they come from the environment?

So, where do microorganisms come from? Do they come from the environment?

Yes!

There is no spontaneous generations. Microorganisms (virus, bacteria, unicellular eukaryote, small multicellular eukaryotes) just like macroorganisms (big-enough to be seen by the naked eye multicellular eukaryotes) are not recreated out of nothing. Abiogenesis happened a long time ago and as far as we know, it is not happening today.

This means that if there is a micro-organism somewhere, it must have come from the environment. It did not pop up out of nowhere.


Help in understanding a sentence about TCR-MHC interaction and immune synapse formation T-cell co-stimulatory and co-inhibitory molecules (collectively named co-signaling molecules) play a crucial role in regulating T-cell activation, subset differentiation, effector function and survival. Following recognition of cognate peptide-MHC complexes on antigen-presenting cells by the T-cell receptor, co-signaling receptors co-localize with T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

I'm not sure I understand the second sentence. The language is a little confusing to me. Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR? Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?
Here's my paraphrase of this sentence:

Following recognition of a cognate peptide-MHC complex on an antigen-presenting cell by a T-cell receptor, co-signaling receptors co-localize with (other) T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

Is it correct?

Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR?

Yes. Other TCRs bind other MHC/antigen complexes and they all cluster together, forming an immunological synapse.

Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?

No. TCR:MHC bind 1:1.
Your final paraphrase is correct.


Is there any possibility of interspecies sexual reproduction in animals like hybridizing plants? Inter-species sexuals are happening naturally. My questions is, whether it may lead a creation of new species? This question arises, because of the appearance of Pillayar in hinduism. Please clarify, whether it is possible to create a new species with the appearance of "Vinayagar" that is human body with elephant face.

The answer is : A big NO.

Naturally, there is no way possible to create a species like vinayagar. Humans and elephants are totally different, they belong to totally different orders. And success rate of inter-species reproduction is rare for even species from same family but from different genus.


How to identify a coiled coil from the amino acid sequence? I was wondering, when we have an amino acid sequence, is it enough to check whether the positions a-d correspond to hydrophobic amino acids in order to say whether it can form a coiled coil structure? Or would we need to make sure the other positions are not hydrophobic too?

All help greatly appreciated.

The heptad repeat, denoted [abcdefg]n, typically has hydrophobic residues at a and d, and polar/charged residues at e and g.

From here.

There is a prediction tool with useful images here.


What kind of lichen is it? I found that in a monastery garden in Czech Republic this winter. I tried to search it on the internet but unfortunately I didn't find it.

I'm pretty sure that it is a cup lichen from the genus Cladonia. A probable species is Cladonia pyxidata, which is relatively common across Europe. My lichen knowlegde is rusty though, and Cladonia is rather species rich with several species that are relatively similar.

(C. pyxidata, pic from http://fungi.myspecies.info/taxonomy/term/4557/media)


What is the substance that tumors release that stimulates growth of blood vessels but suppresses its release from other tumors? I'm currently in high school and I am working on a cancer research project. My project consists of a cancer, and different ways to treat it. I have a set of benign tumor and I was thinking of immediate way of treating it without using a drug like Taxol to destroy parts of the cell is to simply remove the tumor.

However, I remembered learning about a 1 1/2 years ago about a substance that tumors release to stimulate the growth of blood vessels towards them, but this same substance suppresses the release of itself by another tumor (hopefully this makes some sense). I made some drawings that are attached here:

Scenario 1: The 1st tumor in the blood flow releases an unknown substance, which promotes blood vessel growth, but suppresses the release of the same substance from another tumor behind it.

Scenario 2: The 1st tumor is removed, and now the 2nd tumor starts to release the substance, because the 1st tumor's release is not suppressing the 2nd tumor's release anymore.

Does anyone know the name of this substance, and can someone help me learn more about it? Thanks.

One very important signal for angiogenesis are the Vascular endothelial growth factors (VEGF)  (a small group of ~5 similar proteins). They generally promote generation of new blood vessels & migration of these towards the source of VEGF expression.
Blocking VEGF signalling (mostly be blocking the receptors with antibodies) has been a pretty good strategy in cancer treatment, since tumors can't grow over a certain size without blood supply by new grown vessels.

However, I am not aware of any blood-vessel specific signalling mechanism that stops it's own expression at a secondary site. (This may be possible though, especially for specific signals)


Rosette formation: in which order are leafs created From the picture below, it seems that new leaves are formed something like this (if you imagine the plant as a regular, 12 hour clock):

new leaf at 12 o'clock, then at 7 o'clock, then at 2 o'clock, then at 9 o'clock, and so on.

I imagine it could be some things as simple as 'always add 190 degrees'. Are the exact rules for this documented somewhere for various plants?

Spiral Phyllotaxis and the Golden Angle

The disposition of the leaves in your picture is not as simple as it seems. That's a spiral phyllotaxis, which can be very complicated.

The plant in your image is a houseleek, a plant from the Genus Sempervivum.
In those plants, according to Jeremy Burgess (Introduction to plant cell developmnent):

  ... leaf primordia are separated from each other in an angular arc that approaches 137°.

By the way, 137° is (almost) the golden angle (φ).

Here is an image explaining the phyllotaxis of Sempervivum (from Burgess, 1989):

Even more interesting is the pattern made by the 137.5° GA spiral of Aloe polyphylla:

Sometimes this can produce invisible spiral patterns, a phenomenon called parastichy:

Source: Burgess, J. (1989). An introduction to plant cell development. 1st ed. Cambridge [etc.]: Cambridge University Press.

PS: I know that this is off-topic, but I'd like to share this video from Cristóbal Vila, which deals with Fibonnaci sequence, golden ratio and golden angle in nature. Look at the flower disposition at 1:44 : https://www.youtube.com/watch?v=kkGeOWYOFoA


Do butterflies see behind? Butterflies, like many other insects, understand that I am getting near from behind. How do they feel this - through vision, hearing, or some other sense?

Short answer
Butterflies can see behind them.

Background
Merry et al. (2006) have estimated the field of view of the butterfly, by investigating the Orange Sulphur butterfly (Colias eurytheme):

Colias eurytheme. Source: Massachusetts Butterfly Club

The authors found that this butterfly has a very large visual field, encompassing
93% of the spherical space around the animal. There was a small blind spot behind the head not seen by either eye. Another study by the same group showed similar results in another species of butterfly, the Empress Leilia (Asterocampa leilia). Here is a picture of the estimated binocular field of view of the Orange Sulphur, revealing that the animals' vision is virtually spherical, with only a small blind spot at the back (the white area):

Source: Merry et al., 2006. Grey is the field of view, white the blind spot posteriorly. Cardinal directions are indicated (Dorsal, Ventral, Posterior, Left and Right).

Here are a few pictures of other species of butterfly that show the protruding compound eyes covering a large field of view:

Sources: Alex Sukonkin and PhotographersDirect

The feature of large visual fields in insects is, however, not restricted to butterflies (Lutowski & Warrant, 2002). Another insect I often try sneak upon to take pictures are dragon flies, and more often than not they fly away regardless of the angle I approach them. They too have these large compound eyes with a field of view extending to the back:

Source: Nature North

References
- Lutowski & Warrant, J Comp Physiol 2002;188:1-12
- Merry et al., J Insect Physiol 2006;52:240–8


How do we know the presence of light when our eyes are closed? Last night I laid on my bed and tried to go to sleep with the light off.
I closed my eyes (but hadn't gone to sleep). My younger brother touched the wireless mouse (which had laser) for the laptop.  He wiggled the mouse and it's laser contacted my closed eye . I knew some light was thrown on my face, and it's color was red. The laser on the mouse was actually red. So my question is, when my eyes are not functioning (not seeing, closed) how did I come to know that there was a light aimed at my eyes, and it was red?

Short answer, your eyelids does not block all light. Since they are only a thin layer of skin, the light is able to pass through although not completely obviously. Since the eyes are still completely functional when you close them, only covered by the eyelids, you are able to see when light strikes your face.


Are there plants that produce (audible) sound? Are there any plants that are at least able to produce some sort of sound? Actively, I mean - depleting energy reserves to produce an audible output, preferably with no experimental amplification. Ultra- or infrasound is also ok.

Edit: I guess a different way of asking this is, "Are there any plant parts whose function is to produce sound?"

Plants make noise all the time as they transport water but that is believed to be an unintentional by-effect. As to the possibility of plants intentionally making noise,
my intuitive answer was no but I might well be wrong, there is actually increasing evidence that plants might produce vibrations for communication.

Two examples: Gagliano (2012) discovered that young maize roots subjected to a 220 Hz sound (check out the figure, not sure if I'm allowed to copy it here) grow towards the sound source and additionally emit periodic bursts of sound themselves for as of yet unclear reasons.  Gagliano, Renton, et al. (2012) demonstrated that chili plant seedlings grow faster in the presence of an adult fennel plant even though this adult plant was isolated in a such a way that it could not communicate via any known mechanism (chemical, light) with the seedlings, indicating influence through an unknown mechanism. The authors consider both magnetism and sound as possible unknown communication methods.

I don't think any of these sounds would be audible for humans though.

Acoustic emission analysis and experiments with physical model systems
reveal a peculiar nature of the xylem tension.
Laschimke, R., Burger, M., & Vallen, H. (2006).
Journal of plant physiology, 163(10), 996-1007.

Towards understanding plant bioacoustics
Gagliano, Monica et al.
Trends in Plant Science , Volume 17 , Issue 6 , 323 - 325

Out of Sight but Not out of Mind: Alternative Means of Communication in Plants.
Gagliano M, Renton M, Duvdevani N, Timmins M, Mancuso S (2012)
PLoS ONE 7(5): e37382. doi:10.1371/journal.pone.0037382


What happens to a human body once a sugary snack is consumed? I'm looking to understand the effects of sugary snacks and/or drinks on a human body. I'm particularly interested in the timing of the ingestion versus various hormonal levels that may be circadian in nature. Is the release of insulin circadian in nature?

Scenario 1:
A person eats 50 grams of trail mix- raisins, sugared pineapple, sugared mango.
What happens in the next couple hours?
Which hormones get released and for how long?
Does the timing of ingestion produce different effects (ex: consumed at 11AM vs 3PM vs 8 PM?) on the body?

Scenario 2:
A person eats 100 grams of trail mix and drinks a can of sugary nectar (48 grams of sugar dissolved in water).
Will this cause the sugar "crash"?
Is there some grams per kilogram of weight guideline on how much refined sugar or corn syrup a human body can handle at once?

Thank you for your response or any keywords that may help me search for this information!

The human/animal digestive tract breaks down food chemically (with low pH/acid), enzymatically (like proteases and glycolytic enaymes which break down protein and sugars respectively), as well as symbiotically (bacteria participates in the breakdown of some compounds in the gut).  The results are released into the blood stream for the most of the body to assimilate.

With foods with complex carbohydrates (scenario 1), the results can be only a modest change in the glucose level in the serum.  This depends upon the specific food which you can understand better by researching the 'glycemic index'.  Highly glycemic foods result in rather short term release of simple carbohydrates glucose/sucrose into the blood.  Lower glycimic food contain complex carbohydrates (which are elaborate chains of sugars) which need to be broken up into simple carbohydrates before they are metabolized the the cells.

Foods which contain a lot of simple carbohydrates change the sugar levels in the blood nearly immediately and it can go quite high.  simple carbohydrates are monomers or dimers of sugars.  BTW complex carbohydrates have few pictures on the web, but you can imagine them as chains and networks of many many simple carbohydrates linked together.

Not all simple carbohydrates are used by human beings for energy.  For instance the glycosamine in 'joint juice' is the sort that makes cartilidge, which just to show you how different some complex carbohydrates can be. BTW i don't recommend joint juice, just trying to give a familiar example.  Its unlikely that the glucosamine you drink will be directly used for your joints!

So glucose is the energy currency in the blood.  when the glucose level goes up insulin is secreted by the pancreas which tells the cells to take up the glucose for glycogen (internal cell energy storage in a complex carbohydrate) or to be metabolized directly.  Diabetes results when insulin is not produced (type I) or when the cells stop responding to insulin (type II).

Human tolerance to glucose in the blood is estimated to be up to about 100 mg/dl long term. higher than this on the average is not healthy and can go up to several hundreds and cause lots of degeneration in the kidney, liver, and eyes, and more.  Exercise and fasting increase insulin sensitivity and athletes have blood glucose that is quite low even if they have a sugary beverage.

hope this helps - many keywords embedded within...

One last note.  Fructose, which is about 45-60% of high fructose corn syrup (the rest is sucrose) is almost entirely metabolized in the liver.  This is why fructose can be harmful to people who drink too much sweetened beverages.  With the liver taking in the vast majority of fructose, it tends to make fat out of it, sort of overdosing it to make it fatter than the rest of you relatively quickly.  Fatty liver is a marginally disfunctional liver and can cause health problems down the way.  Abdominal body fat (not on your love handles, but amongst your chest cavity and internal organs) is particularly harmful as it interferes with all sorts of organ function.  Probably something everyone should be aware of.


Do proteins contain phosphorous? If its true then how alfred hershey and martha chase used the statement that proteins do not contain phosphorous? I hv heard about phosphorus that it is a constituent of certain protein, although we know that no amino acids have phosphorus... and if its true then how Alfred hershey and Martha chase experiment got acclaimed whose base of the experiment was that "protein doesn't have phosphorus"??

Yes some of the proteins contain phosphorus but in the experiment (Hershey and chase experiment) they used bacteriophage it's protein sheath contains carbon,hydrogen,nitrogen and sulphur while the DNA in the bacteriophage contains carbon,hydrogen,nitrogen and phosphorus(in the acid) so they selected this for that experiment moreover sulphur is absent in the DNA but phosphorus is not so one can conclude that DNA is the thing that was transferred
Reference:NCERT


gene expression of tumor with different percentage of infiltrates I'm performing differential gene expression analysis on rnaseq of  tumor samples that might have different amounts of immune infiltrate.
Tumors are extracted from patients that respond/not respond to immunotherapy

In my lists I found several immune response related genes significantly modulated but i suspect that this could be related to the different amount of immune infiltrate.
In order to highlight the genes that are induced by the tumors and not by the different amount of immune cells... it could be appropriate to normalize the raw reads counts (on which is based my analysis) on the basis of CD3 gene?

Consider that while a fair portion of your immune infiltrate will be T cells, that you can also have dendritic cells, macrophages, B cells, NK and NKT cells, and other cell types. I like to use this figure to demonstrate that fact, and also make note that the relative abundance of immune mRNA by cell type differs by indication (figure 1).

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852857/

Also consider that for T cell markers like CD4 or CD8, these are expressed by antigen-presenting cells, as well.


What is a microsome? This site says:

  In cell biology, microsomes are vesicle-like artifacts re-formed from pieces of the endoplasmic reticulum (ER) when eukaryotic cells are broken-up in the laboratory; microsomes are not present in healthy, living cells.

Whereas this other site says:

  Microsome is another name for the smooth endoplasmic reticulum (ER).

Are they both correct? Which one is correct?

The first quote is correct. 'Microsome' is more of a lab term. This is because, as said they are found (re-formed) after centrifugation and as such aren't seen in an intact cell. Differential centrifugation is a technique used to separate cellular constituents into fractions. To quote,

  The microsomal fraction is the pellet produced when the postmitochondrial supernatant is centrifuged at 50,000g for 60 minutes. Microsomes are small vesicles enclosed by a biological membrane. During centrifugation, the endoplasmic reticulum is fragmented into microsomes

The microsomal fraction may also contain pieces from the plasma membranes apart from those from the ER.


What is the "stimulus" that initially triggers an action potential? There are many steps detailing the depolarization and repolarization of axon nodes to describe how an action potential is transmitted from a neuron. But, after looking at many different sources, I still see one clear thing missing: what causes the action potential in the first place? Every source simply says something vague like "stimulus" or the ever redundant "depolarizing current." But, how is this stimulus generated, and what exactly does it do to which chemical to start the chain reaction of moving sodium ions to create the depolarization in the first place?

There are several possible answers, which is partly why the sources you are reading are being vague: they are discussing the chain of events that happen after the initial depolarization, the source of which doesn't matter much for that chain of events.

Receptor potentials

Sensory receptors consist of some machinery that eventually lead to ion channels opening, often cation channels. This machinery can be direct, where a stimulus directly opens an ion channel, or it can me mediated through g-protein coupled receptors. There are many many examples, but one favorite toy example is the TRPV1 receptor, part of the "transient receptor potential" family.

TRPV1 channels open when exposed to high temperatures or chemical agonists like capsaicin (which gives chili peppers their 'heat').

There are mechanically gated channels in the inner ear that are stretched open as sound waves pass; there are G-protein coupled receptors in the retina that are activated in response to light - when they are activated, they close channels which reduces neurotransmitter release and therefore changes the amplitude of the post-synaptic polarization.

Ligand-gated ion channels

Synaptic transmission between neurons is often mediated by ion channels that are gated by neurotransmitters. A presynaptic cell releases a neurotransmitter, for example glutamate, and that neurotransmitter binds glutamate receptors on the post-synaptic cell, for example AMPA receptors. These receptors are non-specific cation channels, and when they open sodium comes in and depolarizes the cell. Other neurotransmitters, including inhibitory ones, work a similar way.

Gap junctions/eletrical synapses

Although they only occur between particular populations of neurons in mammalian nervous systems (for example, some inhibitory networks in the brain and between cardiac myocytes), some cells are coupled through channels that allow ions to pass between cells. Therefore, depolarization in one cell can be transmitted by ions flowing through that gap junction and begin to depolarize the adjacent cell.

Intrinsic conductances

It doesn't really apply in the context of a "stimulus" but in some types of cell there are intrinsic conductances that can bring a cell to threshold and trigger an action potential. One example would be in the pacemaker cells of the sinoatrial node that initiate cardiac contractions.


Why do nerve cells convert electric signals to chemical signals? One would assume that a faster response time in the nervous system would be beneficial. However, nerve cells have to convert electrical impulses to chemical signals and cross a synapse. Why didn't nerve cells evolve in such a way as to transmit signals purely electronically, and what was the evolutionary need for the current, more complicated structure of the nerve cell?

I've seen answers on how synapses ALLOW for more complicated structures, but never how the synapse came to be. Is it even possible to have a brain structure without converting between electrical and chemical signals? If not, why not? If so, why synapses?

There are two types of synapses:

Chemical synapse
Electrical synapse

The first one is the one you are asking about.  The second one corresponds to the faster synapse you are imagining. It consists of two neurones connected by a gap junction. Gap junction form a cytoplasmic bridge between the neurones and thereby allow electrical signal to directly go from one neuron to the next through ion diffusion without converting to chemical signal.

The second one implies release of chemicals (neurotransmitter) in the synaptic cleft, the extracellular space between the two neurons. It is indeed slower than the electrical synapse. However, unlike the electrical synapse, it enables a variety of postsynaptic effects. Some neurotransmitter elicit excitatory effects, some elicit inhibitory effects (electrical synapses where the presynaptic side is an axon only allow excitatory effects). Some postsynaptic receptors to neurotransmitter are ionotropic whereas some are metabotropic. The former are neurotransmitter-gated ion channels, which means that they let specific ion cross the postsynaptic plasma membrane when they bind neurotransmitter. The latter trigger intracellular chemical reactions, such as production of cAMP, which is a companent of a signalling pathway and can for example influence the expression level of specific genes.

This more diverse set of postsynaptic response enabled by chemical synapses explains why they dominate our nervous system.

Reference: Purves et al., Neuroscience, 5th ed., 2012 ISBN 978-0-87893-695-3


Do species ever go extinct by becoming too successful? Are there examples of species that have driven themselves into extinction by being too good at what they are doing? Like a predator that evolves to hunt so efficiently that it kills all it's prey and then goes extinct itself.

yes, infectious bacteria are a good example, a highly destructive infection may often kill its host before it can spread the disease.  https://www.ncbi.nlm.nih.gov/books/NBK27114/


When does meiosis occur in flowering plants? At what point does meiosis occur during the development of a flower?

In case of male gametophyte (in angiosperms), meiosis ends before the formation of the pollen tetrads which in turn marks the end of cell division in anthers and petals (Li and Johnston, 1999). However, the same study reveals that the relative timing of pollen tetrad formation with respect to floral development (abbreviated as RAFT), varies between different plants. Despite the variation, they seem to form three clusters with mean RAFT at 0.45, 0.62 and 0.73.

In case of the female gametophyte, the megasporogenesis happens inside the ovule (Yadegari and Drews, 2004). Therefore, ovule should have formed before the onset of meiosis. I could not find a detailed study on the timing of the megasporogenesis.


Has lamarckism been discredited? Lamarckism is a pre-darwinian theory according to which an organism's traits acquired to adapt to the environment are passed onto its offspring. A couple of years ago, I attended an event with Richard Dawkins and Jerry Coyne, both preeminent evolutionary biologists, in which I remember them agreeing that it is basically B.S. and that acquired traits don't get passed but instead propagate themselves through natural selection. As a non expert in biology, it does not make sense to me that acquired traits would make their way into the genotype and then get passed on, which coincides with what Dawkins was saying. But I am a non expert.

I also have read a few things about epigenetics and it sounds strangely similar to lamarckism. Steven Pinker also discusses all these things in The Blank Slate and he gives a notion that thare is some idealistic ideology behind promoting ideas that we can radically change an organism by environmental conditioning and "save" those changes into the genotype. He says that ideology is to justify government programs aimed at rapidly enhancing mankind whereas natural selection, which proponents of such ideas may deem reactionary, simply is not so optimistic.

My questions are:

Is lamarckism, or inheritance of acquired traits, been conclusively discredited?
What does lamarckism relate to epigenetics

The question is interesting at many levels. Of course, in biology and in any other science there is no absolute or 'objective' truth about some given phenomenon if we really care to look at the nuances. Lamarck seems to be vindicated mainly by a wave of empirical work on patterns of transgenerational inheritance, particularly in the field that is known as epigenetics. You can read a good intro-level review here for some recent developments, some particular examples here, or a more conceptual reading here.

As an evolutionary biologist myself, I will say that most other biologists acknowledge that epigenetics and transgenerational inheritance are important and have solid empirical support, but (for various reasons) some of them are hesitant of calling that 'Lamarckian'.

By the way, Dawkins was a very effective science popularizer, but he does not practice science nowadays, and many of his ideas lie in what is known as 'scientism', which is a blind confidence in science as an absolute truth that is inflexible. The same applies to many positions of Steven Pinker, deGrasse Tyson, etc.


Is the term 'allele' specific to sexual populations? I had always thought that 'allele' simply meant a variant of a gene and thus could be used in the context of either asexual or sexual populations. With it only being slightly less useful as a concept in asex because of the lack of recombination and thus no reshuffling of allele among offspring. Recently, I was reading a paper that wrote:

  In the asexual and sexual populations mentioned earlier, the implicit model space is simply a point in genotype frequency space or allele frequency space, respectively.

Suggesting that alleles should primarily be used in the context of sexual populations. Wikipedia gives a general definition consistent with both asex and sex use, but all examples listed are sexual.

Hence my terminology question:

Should I use the word 'allele' for variants of genes only in the case of sexual populations? Or is it alright to use 'allele' in populations of obligate asexuals?

I realize why recombination forces us to represent a whole population as allelic frequency instead of talking about individual genotypes, and why asex lets us focus on just the latter. In this question, I am not curious about this distinction, just the purely terminological question.

No, it's fine to use for asexuals too. There's an ambiguity in the term "locus" for asexuals, but "allele" is fine, and "gene" is not much more ambiguous than it is for sexuals (which isn't saying much).

Your final paragraph seems confused though, and I think it's related to your main question. When recombination is sufficiently frequent to keep the population in linkage equilibrium, it allows us to represent the population simply as a point in allele frequency space, rather than in the full, exponentially-larger genotype space. So Watson and Szathmary are using different terms for the two cases not because they can't use "allele" in an asexual context, but because alleles are not sufficient to describe an asexual population.

In general sexual populations are not in linkage equilibrium and cannot be simply described by allele frequencies either, as W&S note later in that paragraph.


Draw simplified phylogenetic tree for kids I need to draw simple, phylogenetic tree for kids lecture.

I am looking for an online tool where I can enter organisms (e.g., human, wasp, fungus) and get figure of a phylogenetic tree. Tree should be based on how close those organisms are (I don't need genome alignments).

Similar figure producing tool would be perfect.

As per your requirements I will suggest:

http://www.onezoom.org/


How did the nucleobases in the Murchison meteorite form? The Murchison meteorite is an important piece of evidence for abiogenesis, because it contained nucleobases from extraterrestrial origin, as this Wikipedia article explains.

  These results demonstrate that many organic compounds which are components of life on Earth, were already present in the early solar system and may have played a key role in life's origin.

My question is: How did these nucleobases arise? Is it possible for these nucleobases to have been synthesized naturally from simpler molecules in a specific environment, like in the Miller-Urey experiment for amino acids?

It is interesting to note that, in the Wikipedia article, it states that

  The amino acids were racemic (that is, the chirality of their enantiomers are equally left- and right-handed), indicating that they are not present due to terrestrial contamination".

This implies that, if a 'life form' did create these proteins, they are fundamentally quite different to life on earth. (Particularly in light of the 70 unique amino acids they described!).

We cannot ever 'know' how they were made, unless a pretty revolutionary discovery is made that undisputably confirms evidence for extra-terrestrial life (although this is the best evidence yet!), so we are left to speculation.

The nucleobases either formed 'randomly' in one of the countless celestial events (although the chances of this seem pretty remote given the complexity of the molecules and the homogeneity in the sample), or they were made by extra-terrestrial 'life' (much more exciting, and indeed probably more likely, as we will see). (Or the 3rd option: intelligent design, however this is dramatically less probable than either of the other two).

The Miller-Urey experiment to which you refer has been subsequently enhanced, and evidence for the "catalytic potential of cosmic dust" is now reasonably robust (Hill, 2004). They demonstrate that simple nebular iron silicate catalysts can yield methane and water from CO₂ and H₂, and ammonia from N₂ and H₂. Allowing these to react yields nitrogen-containing organics such as methyl amine.

It is not a huge jump to suppose that with enough time, mass and energy, these reactants could combine and form a molecule (chain of amino-acid-like molecules - a protein) capable of faithfully replicating itself, and thus initiate life. There is no reason to suppose that Earth is unique in this respect; there are billions of suns in our galaxy alone, and billions of years of time for these reactions to take place.


How do NSAID's work and what are the differnces between COX-1 and COX-2? NSAID's work by slowing down the COX enzym, but how do does enzymes cause pain? because I've read that they're also needed for the body and do "good" things.

NSAIDs work by inhibiting COX-1 and/or COX-2. These are the key enzymes in prostaglandin biosynthesis. Prostaglandins act as messenger molecules in the process of inflammation and therefore can cause pain and other inflammatory symptoms. Source

COX-1 is normally present in different tissues of the human body and is for example important for maintaining the stomach lining. By contrast COX-2 mediated prostaglandin synthesis is only induced by injuries and inflammation. The analgesic effect of NSAIDs is therefore mainly based on the inhibition of COX-2.

There are to different classes of NSAIDs, non-selective (aspirin, naproxen, ibuprofen, ...) and COX-2 selective (celecoxib, parecoxib, ...-coxib). Due to the different roles of COX-1 and COX-2 these different drug classes have different adverse effects and differ in their analgesic effect depending on the dose. E.g. use of aspirin can lead to ulcers of the stomach or duodenum while COX-2 selective drugs do not cause gastric problems (but others).


How to get rid of mosquitoes in a small lake I own a small lake. Give or take it is about 50 meters wide and 100 meters long (or 160 feet wide, 320 feet long), with a max depth of around 2 meters / 6.5 feet. One third of the lake is surrounded by forest, the rest is grass / small enclaves of tress. The lake absorbes only rainwater from the surrounding residential area. There is a small outlet towards a much larger lake close by. The lake was recently dredge to remove many years of plantlife that had almost turned it into a swamp.

The lake has a large number of mosquitoes. There is also quite many frogs and a few birds that live near the lake.

What can I do to decrease the amount of mosquitoes in the lake?

For example, can I set up certain nesting boxes that will attract birds or bats that will eat a large number of mosquitoes?

Can I release certain fish that thrive on mosquites?

It is in Scandinavia.

EDIT

The shorelines are sharp and most of the vegatation has recently been removed. The lake was recently completely emptied and about 2 meters (or more) of vegatation and soil was removed. The lake has previously been contaminated which was cleaned away. I guess this means that a very large part of the ecosystem has been removed, a few fish did manage to survive, but not very many.

There are a number of environmentally destructive methods that would be effective, including draining the lake, covering the surface with a continuous layer of oil, or adding toxins to the water, but I'm assuming you're looking for a method that will have the minimum possible off-target effect.

Different mosquito species breed in different habitats and are thus susceptible to different control strategies, so good photos of some adults might help, but I'm assuming here that you've correctly identified the lake as the breeding site. If there are any other possible breeding sites in the area please add them to your question.

If the assumptions above are correct then, broadly speaking, your best options are habitat modification or biological control. I'm not going to go into chemical control here since as stated above I assume you want low environmental and financial cost; if this is incorrect let me know.

Habitat modification: regularly removing
plant growth within the lake and trimming vegetation overhanging the edges will limit the ability of mosquito larvae to escape predators and may have some effect. However, the recent management you describe has
probably gone some way towards this (did you
notice whether the mosquito problem got any better after the plants
were removed?)
Biological control: introduce predators or parasites into the environment. Plenty of species eat adult mosquitoes but there aren't really any that primarily feed on them (unless they're the only food source available) and many adult mosquitoes will have laid eggs already - the most effective strategy will be to target the immature population. Larvivorous fish have been shown to be effective in many parts of the world, for example fish in the genus Gambusia ('mosquito fish'). I don't know of any that have been shown to be effective and can thrive as far north as Scandinavia, but if you stock the lake with fish (combined with managing vegetation as above) I'd be surprised if you don't see some improvement.
Biological control, part 2: Use Bti (Bacillus thuringiensis var. israelensis). This is a bacterium that produces toxins which are highly specific to dipterans and don't really affect anything else. You can buy the bacterium in various formulations including sprays, tablets etc. I'm mainly familar with its use for controlling container-breeding mosquitoes, but this paper describes its use in large lakes so should give you some idea of dose required, optimal application method and time to reapplication.

Without knowing more about your budget, available time/manpower etc I can't really help you choose between these but I suspect #3 is your best bet.


Parasitism and mimicry I was reading this article which states this:

  Classical Batesian mimicry, in which an undefended mimic evolves to
  look like a toxic model, is a parasitic relationship in which the
  mimic gains an advantage at the expense of the model

I don't understand why this mimicry is equivalent to parasitism. Do the authors call it parasitic because eventually it may cause threat to the model, as the predator learns that it is being fooled around ?

I don't see a clear and certain antagonistic relationship here. Can someone please explain.

EDIT

If it is the case that the mimic reduces the likelihood of the model being preyed then then outcome of this is dependent on multiple parameters.

The +/- effect of this interaction is not always certain (which on the other hand is usually certain in the case of a typical parasitism). The uncertainty can arise not just by evolution of the predator but by other factors such as population size and structure.

Considering all this is it correct to call a relationship as parasitism just based on one of the many possible outcomes ?

A parasitic interaction is when one species has a fitness increase (benefit) from the interaction while the other has a fitness decrease (cost). Note: you don't need to have physical contact to have an interaction. As soon as the presence of one specie influence the fitness of the other, it is enough to consider that there is an interaction.

In the case of Batesian mimicry, I think it is obvious to understand why the non-toxic species gain from this interaction. Let's imagine the toxic (model) species is blue. Predators learn to avoid blue species because they feel very sick right after eating it. In other words, the predators have a bad experience or even better we can say that the predator receives a punishment or a negative reinforcement (instrumental conditioning). In consequence the predator that got this negative reinforcement will probably avoid blue individuals in the future.

When a predator eats an individual from the mimic non-toxic species, he got a positive reinforcement. In consequence the predator learns that the prey tastes good and in consequence it is more likely to eat a blue prey next time it encounters one, which obviously has a negative impact on toxic model organism.

Now, I have two issues with this concept.

The interaction is not one-to-one and we can consider that the presence of a species that use Batesian mimicry influence the variance in fitness of the toxic species only if (actually you might argue differently by not assuming infinite population size) the distribution ranges are not completely overlapping or if there are some kind of population structure.
If the toxic species causes death to the predator, then the predators never get the opportunity to learn. But one can consider the same mechanisms at evolutionary timescale than at the time of the lifespan of the predators. It is also possible that the predators have higher cognitive abilities allowing them to gain insights concerning the toxicity of one species without having to taste it.

EDIT

  What if predators can tell the difference between the two prey species?

Your point, if I understand it, is that if the predators manage to sense (or to evolve sensing) the two prey species differently (in consequence the non-toxic species does not mimic the other prey species anymore), then the toxic species will not suffer anymore from the mimicry. So in other words, mimicry is a parasitic interaction but predators might evolve ways to sense the two species differently in which case there would have no mimicry anymore. Note: the predator is more likely to evolve good sensing abilities if it forages on few species only.

I think your issue is that you should not consider a species to be mimicry if the predator can tell the difference between the two prey species. It is not to the human eyes that the mimicry makes sense but only to those of the predators. So, batesian mimicry is a parasitic interaction and if the predators evolve so that they can sense the difference between the two species, then there is no more Batesian mimicry and there is no more parasitic interactions between the two prey species.

  Why do you say that  "physical contact" not necessary for two species to have a parasitic interaction?

The interactions between species are defined as follow:

The benefits and costs (harmed) are defined in terms of fitness. These definitions do not involve any physical interactions. And to the eyes of the evolutionist at least, that would not make much sense to add a notion of physical interaction into these definitions.

  In the case of Batesian mimicry the ± effect is not always certain (while it is certain in common parasitic interactions)

The point is interesting. I think it just mean that the non-toxic organism is a facultative parasite (a species that can live with or without the parasitic interaction). Statistically speaking, if you have enough preys of each species and especially enough predators, then the consequence is certain.

Consider the common Ivy. It is a parasite of other plants but can also live on human-made walls in which case the negative effect on other plants is not always certain either. The difference between the Ivy and the non-toxic prey is that the fitness of the non-toxic prey depends on whether it parasites the other species while the Ivy is doing just fine on human-made walls.

You can think about the interactions between rabbits and wolves. They share a prey-predator interaction which is a special case of the parasitic interaction according to above diagram. In a particular environment the wolves might be absent and so predation does not occur, just like the non-toxic species might be absent species might be absent and so the parasitic interaction does not occur anymore.


What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking? We know that software tools like I-tasser etc have a web server and a standalone option too. Is there any difference to protein C-scores or efficiency or accuracy if you do it on standalone instead of web server?

What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking?. Available from: https://www.researchgate.net/post/What_would_be_the_difference_if_I_use_the_Web_server_instead_of_dedicated_server_for_protein_modeling_and_docking [accessed Apr 27, 2017].

There should be no difference in output.*** The big difference is likely going to be in the size of the analysis you can perform, and how fast the analysis is performed. A lot of web-servers have a job size limit to prevent one person from hogging resources unless you buy greater access. On a public web-server, your job is queued with everyone else's. If the server is in high demand, you may have to wait along time for your analysis to kick off.

***: I said there should be no difference in output and that is true if you set up your server the same as the public webserver with the same parameters used for analysis execution. This could be a good or bad thing depending on what you are trying to accomplish. Some public webservices do not give you access to all parameters, so setting up your own may give you the ability to tune your analysis to a greater degree.


What is the difference between the cellular affix -cyte and -blast? The affix -blast means an immature cell, and -cyte indicates any cell. So how do we define if a cell is mature (-cyte) or immature (-blast)? How does this apply to odontoblasts and ameloblasts? Why are they not simply called odontocytes and amelocytes, respectively?

What are the criteria for using the affix -cyte versus -blast?

Short answer
 - The affix -cyte means cell;
 - The affix -blast means a germ (bud) cell or a cell that produces (building) materials.

Background
Cells are denoted as -cytes. There are many of them, e.g. melanocytes in the skin and chondrocytes in the cartillage.

Germ cells are denoted as -blasts. These cells typically are precursor cells such as the lymphoblasts that are undifferentiated precursor (stem) cells situated in the bone marrow that produce leukocytes.

Blast cells may also be cells that produce materials. Your examples are of that category; odontoblasts generate dentine, the main hard tissue of the tooth; ameloblasts deposit tooth enamel, which is the hard outermost layer of the tooth forming the surface of the crown. in that sense, also progenitor cells produce something, namely new cells. Hence, blast cells are cells with a chief building function, either materials or new cells.

There are also -clast cells - cells that destroy something. Fig. 1 below gives an overview of these cells as present in the bone, namely osteoblasts (bone builders that secrete the matrix), osteocytes (osteocytes are osteoblasts that are embedded in bone; they stop secreting matrix and only maintain it) and osteoclasts (different class of cells that mediate bone resorption).

Different cells in the bone. source: University of British Columbia

Why then do not call odontoblasts odontocytes? - Because it would mean loss of information. It would be the same as calling a car and a bike both transport vehicles. Moreover, the example in Fig.1 is quite convincing, as osteocytes and osteoblasts are considered to be different cells altogether (although the former is derived from the latter).


Most painless method for killing insects I'm planning on having a small farm of crickets or grasshoppers.
I would like to cause them as little suffering as possible, so I'm wondering what is the most painless way to kill them?

So far, the plan is to put them into the fridge (+4C) to slowly chill them (that way they will not notice it as much), and then to freeze them in the freezer (once they are chilled and are either unconscious or barely so).

EDIT: It is important to note that I am planning on eating them.

The terrestrial invertebrate taxon advisory group of the Association of Zoos and Aquariums recommends anesthetizing the insects with carbon dioxide and then placing them in a freezer to euthanize them.


Evolution of Chromosome Numbers Some species have different numbers of chromosomes, as we all know. Throughout evolution, how was a species able to survive with an extra chromosome? How was this organism able to breed successfully to form offspring with the additional chromosome?

Chromosome splits (or fusions for that matter) might not mean that much for reproductive success since genes can still line up and recombine. To quote the science blogger P.Z. Myers:

  [C]hromosome numbers can change dramatically with no obvious effect
  on the phenotype of the organism.

He illustrates it thusly:

So to answer your first question, changes in the number of chromosomes aren't always fatally deleterious (as you seem to think).

As for how a change in chromosome number might spread, the explanation is likely random drift and inbreeding. To quote P.Z. Myers again:

  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant.

"Evolution" by Mark Ridley, p. 361 similarly points out that reproduction will be an uphill battle until the new variant becomes more common (often through inbreeding or drift in small populations):

  When a new chromosomal fusion mutation arises, it will be selected
  against because of its disadvantage in heterozygous form. But if it
  drifts up to a locally high frequency, as may easily happen in a
  local, small, and perhaps inbreeding, mouse population, natural
  selection will favor it. Natural selection favors whichever
  chromosomal form is locally common[.]

This might in the end lead to speciation due to the two populations becoming incompatible.