text:
Would a shark whip into a frenzy from smelling its own blood?
Sharks normally respond very quickly to the scent of blood in up to a mile radius, but what if the shark itself simply got injured? Would it respond to its own blood at all?

That would mean the real question is: why not? How could they automatically distinguish their own blood from that of another shark or fish? Would simply knowing it got injured be enough?

Great question +1

I would think no, given that the shark would detect the blood in such close proximity, and then upon looking around, not see any other sealife. And as for the shark having some sensativity towards detecting its own blood vs others, sharks have no such ability. Also, just as a side note, I believe I had read several articles stating "one mile radius" is actually something closer to "a quarter mile radius", and is greatly dependent on the diffusion rate of the blood as it travels through the ocean currents.

I'm pretty sure, they can smell their own blood, but they do not attack themselves. Wounding a fish results in the release of chemicals into the water. This is a signal for other fish about potential danger and they will escape (Schreckstoff). Of course, the predator of the wounded fish will not mind. So this seems to work best within the same species. Fishermen and military have apparently used dead or rotten sharks in the past to keep sharks from attacking (Shark repellent). I guess, a similar mechanism plays a role here. Sensing a wounded member of the same or close species (including oneself), would block any feeding behavior.
The Myth Busters have actually done this (not very scientific) experiment: https://youtu.be/E1GenfKR9pk

Yes, sadly they do as the smell of fishes blood turns them into a frenzy, as they are fish.But i see no reason the shark would get hurt in the first place.

It is likely not the case that there would be a feeding frenzy if the question is whether a shark would attack an injured member of it's own family or species. The main reason is for reproductive means as a video will explain on this website:
https://sharkopedia.discovery.com/shark-topics/life-cycle/#how-do-sharks-avoid-inbreeding
Although there could be a few exceptions.  Semelparity in female tiger sharks for instance, has been observed.  Information about all sharks pertaining to this matter is difficult to come by.

This doesn't answer the question, which is clearly about the response of a shark to its own blood.

The question is what if the shark itself simply got injured?  Would there be a freezing frenzy?  And the answer I'm suggesting is no.  The shark wouldn't eat itself for the same reason..

They prefer not to fight with members of their own species.

The question is Would a shark whip into a frenzy from smelling its OWN blood?  The first sentence of your answer incorrectly restates the question by ending thus; if the question is whether a shark would attack an injured member of it's own family or species. My initial comment was made so you knew the reason for a down-vote and could consider editing the answer.

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text:
Concerning Rabies can an animal feeding on rabid bat transmit right away?
Playful kitten found biting and toying with a dead bat. Lets say the kitten nips and plays rough with a human right after biting and toying with the bat.
Will a potential rabies virus transmit from the mouth of the kitten into the human being that it may still harbor the virus from the bat?
Putting aside the fact that the rabies virus takes days to weeks to infect the kitten, can the virus cross contaminate from the mouth or nails of the cat if the feline was playing with the corpse?

Yes, there is a possibility that a kitten can transmit the virus if that kitten had fresh infected bat blood or saliva on it's claws or teeth and gets it directly into your eyes, nose, mouth, or a wound. It's very rare and exceedingly hard to prove, however. These are called non-bite exposures.

source: Stack Exchange

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sort: votes


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Why boys who inherit more genes of their mother are not born as girls and girls who inherit more genes of their father not born as boys?
If boys as well as girls inherit the genes of the father as well as mother, does it imply that boys inherit more genes from the father to be boys and the girls inherit more genes from the mother to be girls? Or there is some thing else to it that settles the sex of the children? Since girls may inherit more genes of father and less genes of the mother question arises what decides that they are not born as boys or the other way around why the boys who inherit more genes of their mother are not born as girls?

Related (but a little more advanced): Do males of all sexual species have Y chromosomes? and Does one parent transmit more DNA to the offspring than the other one?

Most genes are not male or female, so receiving more genes from a father or mother would not make a child more male or female. Whether a mammalian embryo grows to be male or female is pretty much determined by a single gene that's found on the Y chromosome. Called the "Testis-determining factor" (TDF), it triggers the development of male characteristics. TDF is a regulatory gene, and its effect is to switch on other genes, which result in the development of testis. All embryos would become female without the intervention of this gene.
The gene TDF is found on the Y chromosome. Male mammals have one Y chromosome and one X chromosome, females have two X. So there's a 50% chance a fertilised egg will inherent an X, and a 50% chance it will inherit a Y chromosome from it's father, which determines its sex.
References:
Testis determining factor, https://en.wikipedia.org/wiki/Testis-determining_factor
General info about sex determination in different animals (it varies a lot),
 https://www.nature.com/scitable/topicpage/genetic-mechanisms-of-sex-determination-314

The second article states that 45,X (Turner syndrome, IIRC) is female, though I didn't see a justification for this. Anyone know if that's correct, and if so, why? To my understanding, Turner syndrome is neuter.

I am assuming that you are asking about human reproduction (which can be generalized for mammalian reproduction).
Humans have $23$ pairs of chromosomes. Of these $1$ pair is known as sex chromosomes. Human sex chromosomes are named $X$ and $Y$. An individual with genotype $44A + XY$ (A denotes the other 44 chromosomes) is a male and an individual with $44A + XX$ is a female.
Ref - https://en.wikipedia.org/wiki/Chromosome#Human_chromosomes
During reproduction the child receives $X$ from the mother and either $X$ or $Y$ from the father. It is the Sry gene on the $Y$ chromosome which gives male rise to male characteristics.
Also there is no such thing as more genes from the mother/father. The gametes (sperm and egg carry equal number of genes from the father and mother.)

Welcome to Biology.SE! Please add some references to your answer.

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Any idea what this fish is?
Bought this Fish at the pet shop today. Forgot it's name.
That pink fish

It might be easier to go back to the pet shop...

Your fish in question is a zebra danio GloFish; they're genetically engineered to have flourescent coloration. The giveaways for me were the shape of the body (minnow shaped, with zebrafish belonging to the minnow family), its size (small), and the striped pattern running along the body, parallel to the lateral line. Since the fish in your picture is in motion, it's a bit difficult to see, but it's definitely there (can be seen closer to the head).

And here's another image, where the coloration is closer to what you have. (IMO, the previous image has a strong contrast, especially with the black background)

This zebrafish is suffering from a bent spine, which accounts for the misshapen body. (source)

Also, it seems that the fish in the background is a black-skirt tetra.

I believe that is a Pink Dottyback.

[Source:Blue Zoo Aquatics]

Seems like your identification is correct. I suggest you add an image from google here instead of telling to double check it.

Also +1 since I had no idea who downvoted the answer.

@user33990 I have added the image for you, but please provide some description of the species that why you think it's correct.

Welcome to Biology.SE! Please add some more details in your answer.

Are you sure? The top fin seems much longer, the shape of the tail is very different, the color of the eye is different. I'm fish biologist, but I have doubts.

If I'm not mistaken, that's a saltwater fish. The tank in the picture, I'm 99.999% sure it's freshwater. Also, I agree with @RHA.


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Are there any alternatives to DNA as the hereditary material on Earth?
I wonder are there hereditary materials other than DNA  deoxyribonucleic acid (may be on different planets).
In addition, I learned in my high school that carbon and silicon are similar. Is it possible to have hereditary materials with silicon replacing carbon.
Why and why not?

Welcome to Biology.SE! What research have you done before asking it here? There are alternatives to DNA on this planet too...

Irecommend picking a single question, either ask about alternatives to DNA in carbon based life or about the possibility to silicon based life. The silicon based life question might be better for worldbuilding than here since it is much more hypothetical.

First of, depending on your definition of life (which is a matter of philosophy, not science) you may even accept as living something that has not heritable information passed onto 'offspring'. But let's consider only those hypothetical life forms who would have heritable information.
Of course, it is possible for different life forms to use some other mean of transferring heritable information. In fact, there are life forms based on RNA instead of DNA on earth (see RNA virus) and it is even thought by many that life first evolved using RNA and not DNA (see RNA world hypothesis).
To go further in this discussion you should have a look at wikipedia > Hypothetical types of biochemistry (I got the link from @RoniSaiba 's answer).

Typically virus, are not regarded as lifeforms as they cannot replicate on their own without a host. But your point about RNA as a heritable molecule is correct.

Exobiologists definitely consider viruses as being living things of interest. Physiologist might not consider a virus alive due to absence of metabolism (although see mamavirus and among others). Note also that saying they cannot replicate on their own without a host is not a very good distinction for defining what is living. Parasitoid wasps cannot reproduce without a host either, yet everyone would agree they are alive. But I agree that not everyone would agree viruses are alive. See this post for discussion.

The post has a top answer, which explains my point in detail. Virus rely on the host to provide the basic molecular machinery they need to replicate; ribosomes for protein synthesis and the metabolism of the host to provide the basic building blocks of life, amino acids and nucleotides. Thus without a host, a virus cannot maintain itself and will be destroyed over time.

I suggest a read of this wikipedia article [Hypothetical types of biochemistry].1
From my understanding of bond energies (which are proportional to the stability of a molecule) it seems that Si based compounds are less thermo-stable. Given how planets form from molten states it is more likely that carbon based life evolves first and outcompetes the emerging non carbon lifeforms.


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Any simulations of four-winged dinosaur flight? (microraptors)
This week's podcast of the BBC's Science in Action includes a section by Rory Galloway (12:20 to 18:30) covering the Dinosaurs of China exhibit currently hosted by Wollaton Hal at the University of Nottingham, and includes an interview with curator Dr. Adam Smith.
The exhibit is of highly detailed dinosaur fossils from Liaoning, China where detailed feather structures were well preserved and have been analyzed in great detail.
One section caught my attention:

Rory Galloway: "The similarity between dinosaurs and birds was far more than superficial though. Eventually a branch of small, theropod dynosaurs evolved into the birds that fly around today. But curator Adam Smith says, if we concentrate on flight alone, it gets quite difficult to know exactly which branch of the dinosaurs actually became our birds."
Adam Smith: "Flight is really important and that’s why it evolves many times. Some of the earliest flying dinosaurs, such as the microraptor actually had four wings, not two."

The Wikipedia article on the Microraptor is quite long and includes a lengthy, technical discussion on just how these four wings might have been used. It seems that it is (currently) generally believed that these dinosaurs had the capability of powered flight, and that they could actually take off from the ground, rather than climb trees, jump, and simply glide.
This is with four wings.
There are many variety of insects with four wings and the two pair are used in a variety of different ways. But these dinosaurs are much larger, of the order of a kilogram.
Question: Have there been any complete simulations of the mechanics of four-winged dinosaur flight, showing how the wings would have been used to take off from the ground and gain altitude? A movie or animation of the coordinated flapping of the front versus rear pair of wings would be great. These days the numerical models and computing power are within reach, but it would still be a substantial effort, so I'm not sure if this has been done yet or not.
I'm assuming that this is not currently believed to be the branch of dinosaur that eventually evolved into modern birds, but it's a fascinating branch nonetheless.
below: from here.

"The similarity between dinosaurs and birds"... that sentence burned my eyes. This is exactly as saying "the similarity between mammals and primates". The fact that he is just a journalist should not be an excuse, because he is a science journalist.

@GerardoFurtado then avert your eyes and relax! In biology, the word "similarity" does not have a precise definition as it does in mathematics. It's perfectly fine to address the similarities and differences between any two things. If you have not listened to the entire segment, 12:20 to 18:30, I'd invite you to do so now, and put the quote back into context as any scientist would. :)

@Gerardo Furtado: No, it's the same as "the similarity between mammals and reptiles".

Apparently both you guys didn't understand it: "birds" is a group inside "dinousaurs". Therefore, the sentence makes little sense, since all birds are dinosaurs. Again: such a sentence is just like "the similarity between vertebrates and frogs", or "the similarity between plants and ferns". You are comparing A with B, however, B is a smaller group contained inside A. That being said, what @uhoh said ("It's perfectly fine to address the similarities and differences between any two things") doesn't apply here, because one of those things (birds) belong to the other thing (dinosaurs)...

... and, regarding what @jamesqf said ("it's the same as 'the similarity between mammals and reptiles'"), that's not the case: mammals and reptiles are two distinct groups, none of them is a clade containing the other one.

@user24284 The author was clearly using the term dinosaur in the popular sense of 'non-avian dinosaurs', not the clade Dinosauria.

Related: https://biology.stackexchange.com/questions/17546/were-there-any-flying-dinosaurs

Note nowhere in the article does it mention the rear wings flapping. The rear wings do not provide lift, they are acting as control surfaces to improve stability and maneuverability. (think of the tail of a plane).earlier/proto flies have far more demand for control surfaces than developed/derived fliers due to lacking more precise control of flight surfaces.
They basically take off just like any other bird, if they could fly. Flight in dinosaurs likely did not even evolve from gliding as we commonly think of it but instead from raptorian pouncing, the sprawled posture of microraptor you sometimes see, with its hind legs spread wide, is anatomically impossible, you literally have to dislocate both legs to do it. Dinosaur hip joints do not allow for much lateral extension unlike mammalian or varanid ones, more like a hinge than a ball and socket.
The animal in flight would have looked like this.

Hall, Justin, et al. "A new model for hindwing function in the four-winged theropod dinosaur Microraptor gui." JOURNAL OF VERTEBRATE PALEONTOLOGY. Vol. 32. 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA: TAYLOR & FRANCIS INC, 2012.

Thank you for setting me straight on the flapping! Searching on the title of Hall et al. immediately gives oodles of open access further reading; ((almost) all pdfs) 1, 2, 3, 4, 5, 6...

The actual original source was part of a conference so all that was physically published was an abstract as part of the conference issue of JVP. This quirk pops up occasionally in paleontology because there are not that many of us and the Society of Vertebrate Paleontology yearly conference is big enough to cover a significant portion of us. So the feeling is if you are interested you will go. There has been talk for years of recording putting the full talks up online but the cost has been a major delay. Like always the media likes the strangers less accurate interpretation.

There is a good attempt at a simulation of 4 winged flight of Microraptor on BBC's Planet Dinosaur.
There's another  Planet Dinosaur video about their venomous teeth and hunting tactics.
And a Microraptor locomotion video on Attenborough's Conquest of the Skies (Sky 3D).

new dinosaur question: Would anything limit an “invasive species” T. rex introduction now besides running out of food or intervention by humans?

Several models have been proposed, challenged, and revised over the past two decades:

Origin of Flight: Could ‘four-winged’ dinosaurs fly?, Nature (2005)

A previously published reconstruction shows that the hindwing of Microraptor supported by a laterally extended leg would have formed a second pair of wings in tetrapteryx fashion. However, this wing design conflicts with known theropod limb joints that entail a parasagittal posture of the hindlimb. Here, we offer an alternative planform of the hindwing of Microraptor that is concordant with its feather orientation for producing lift and normal theropod hindlimb posture. In this reconstruction, the wings of Microraptor could have resembled a staggered biplane configuration during flight, where the forewing formed the dorsal wing and the metatarsal wing formed the ventral one.

Biplane wing planform and flight performance of the feathered dinosaur Microraptor gui, PNAS (2007)

Model tests of gliding with different hindwing configurations in the four-winged dromaeosaurid Microraptor gui, PNAS (2009)
Paleobiology and the origins of avian flight, PNAS (2010)
Distorted Microraptor specimen is not ideal for understanding the origin of avian flight, PNAS (2010)
Additional specimen of Microraptor provides unique evidence of dinosaurs preying on birds, PNAS (2011)
Aerodynamics of the tail in Microraptor and the evolution of theropod flight control (2012)
Aerodynamic performance of the feathered dinosaur Microraptor and the evolution of feathered flight, Nature Communications (2013)
Shifts in stability and control effectiveness during evolution of Paraves support aerial maneuvering hypotheses for flight origins (2014)
Aerodynamic Characteristics of a Feathered Dinosaur Measured Using Physical Models. Effects of Form on Static Stability and Control Effectiveness, PLOS (2014)
The aerodynamics of gliding flight and its application to the arboreal flight of the Chinese feathered dinosaur Microraptor, Biological Journal of the Linnean Society (2014)
HINDWING FUNCTION IN FOUR-WINGED FEATHERED DINOSAURS

new dinosaur question: Would anything limit an “invasive species” T. rex introduction now besides running out of food or intervention by humans?

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text:
Is starch and glycogen digestion intra or extracellular?
Do humans have the enzyme for starch intracellular digestion?
Also, do plants have the ability to digest Glycogen? Intra or extracellular, or both?

In order to avoid people voting to close this as too broad, please pick one question to ask (see my answer below).

The problem with your question is that, right now, you have three different questions:

Is the starch/glycogen digestion intra or extracellular?
Do humans have the enzyme for intracellular digestion of starch?
Do plants have the ability to digest glycogen?

Unfortunately, that goes against Bio SE rules: you have to pick one question, otherwise your post will be closed as too broad ("Avoid asking multiple distinct questions at once.").
That being said, I'll address only this question:

Do humans have the enzyme for intracellular digestion of starch?

The answer is yes. Intracellular digestion in humans (as in any animal) is performed by lysosomes, organelles that contain hydrolytic enzymes.
Lysosomes can digest proteins, lipids, carbohydrates, nucleic acids etc. Regarding digestion of carbohydrates, this is a short list of enzymes (the complete list is way bigger) found in human lysosomes:

alpha-Galactosidase
alpha-L-Fucosidase beta-Galactosidase-1
beta-Glucuronidase Chitinase
Chondroitin B Lyase/Chondroitinase B
Chondroitinase
Cytosolic beta-Glucosidase
Galactosylceramidase
Heparanase
Hyaluronidase
Lysosomal alpha-Glucosidase
O-GlcNAcase
O-Glycosidase

Among the enzymes listed above, this is the one that answers your question:
 Lysosomal alpha-Glucosidase.
That enzyme, which is a α-1,4-glucosidase, breaks down starch (and glycogen) to glucose.
Source:

Lübke, T., Lobel, P. and Sleat, D. (2009). Proteomics of the lysosome. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1793(4), pp.625-635..

DIGESTION IN THE MOUTH:
Starch digesting enzymes are extracellular in human beings.All starches and some glycogen are hydrolysed in the mouth by the time the food is swallowed due to the effect of ptyalin(alpha amylase)enzyme in our saliva.
DIGESTION IN THE DUODENUM OF SMALL INTESTINE:
Pancreatic juice containing pancreatic amylase promotes extracellular starch digestion.And almost all the starch in food is completely hydrolysed to maltose, limit dextrin and isomaltose in its effect.
The same enzyme pancreatic amylase also causes the total extracellular digestion of glycogen in the duodenum and forms maltose and other products like limit dextrin, isomaltose.
DIGESTION IN THE UPPER JEJUNUM OF SMALL INTESTINE:
Products like limit dextrin and isomaltose is digested extacellularly in the small intestine by the enzyme isomaltase and maltose by maltase in intestinal saccus entericus to form glucose.
NATUREOF INTERCONVERSION OF GLYCOGEN AND GLUCOSE IN HUMAN:
The principal glycogen storing organ in human is the liver and glycogen formation or hydrolysis in the organ is 'intracellular'.
NATURE OF INTERCONVERSION OF STARCH AND GLUCOSE IN PLANTS:
Similarly in starch storing organs in plants the hydrolysis or formation is 'intracellular'.
REFERENCES:
https://en.m.wikipedia.org/wiki/Starch
https://en.m.wikipedia.org/wiki/Glycogen
https://www.ncbi.nlm.nih.gov/books/NBK21190/
https://en.m.wikipedia.org/wiki/Carbohydrate_digestion
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.2004.01101.x/pdf

It seems like you're getting confused between starch and cellulose. Amylase digests starch, and is obviously found in humans.

xtremely sorry @ another'Homo sapien'.I 'll edit right away.And thank u really.

"Digestion in the pancreas" really?


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What is synaptic bias?
In non linear model of a neuron there was a mention about bias (Bₖ) which was the summation of the synaptic weights.
I want to understand what synaptic bias is and their application/use in neuronal modelling.

Often artificial neurons are created with conventions that zero is "rest" and 1 is "threshold". The unit starts at 0, and when it reaches 1 it will send an input to all of its targets and be reset back to 0.
This isn't exactly how real biological neurons work, but its a reasonable approximation in some contexts (and can do real world computations).
Most of the inputs to a unit are variable, so you add some voltage to the neuron based on the synaptic weight. For example, one input with a weight of ".2" would move the cell 1/5th of the way to threshold by itself.
When people talk about a bias input, they are referring to an extra "always-on" input with a small synaptic weight. This can maintain a rest greater than 0 in a leaky integrate-and-fire cell; this allows for some more biologically relevant forms of inhibition (negative synaptic weights) to have an influence on the unit, by offsetting the bias input and pushing the voltage back to 0.
More often, I am familiar with using a bias input in networks that are not leaky. These networks just integrate until they reach threshold (although they may or may not get negative inputs). For these networks (or for a leaky network where the bias current is substantial relative to the leak), adding a bias input ensures that the network won't stochastically "fall asleep" due to a period of low activity. If the bias current is equivalent to ".02" units per cycle, for example, you would guarantee that the cell would fire once every 50 cycles with no other input.
There are some real excitable tissues that show similar behavior, but not due to a real bias input. Rather, there are intrinsic channels that slowly depolarize a cell. Some examples are in cardiac myocytes and the sinoatrial node making up the heart's "natural pacemaker", as well as in brain circuitry that controls breathing. The bias input is sort of a "made up" construct that is functionally, but not mechanistically, correlated with real biology.


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Concentration calculation of Factor VIII for Elisa
I have the following problem. I'm trying to get the concentration calculation for an Excel sheet that will calculate values from an Elisa plate.
The basis is a standard curve with the following values:
Std: PreDil factor 1: 40
PreDil factor 2: 55
---> Total Predilution = 2200
Concentration: 2123  µg/ml
Dilution  1:20      1:40    1:80
Std 1     1,3910    0,6360  0,2850
Std 2     1,4020    0,6360  0,3140
Std 3     1,3500    0,6250  0,2880
Std 4     1,4470    0,6810  0,2900
The sample values are the following:
Predilution: 15
Dilution 1:20   1:40   1:80
Sample   0,4060 0,1940 0,0760
According to the program that has been in use earlier, the concentration shall become 4,786 µg/ml. How do I calculate this in the best way? Unfortunately, I can't seem to get the right answer.
To add more context to the question. I work on a project to move an old program that calculated the concentrations to a new excel sheet. Unfortunately, I do not perform these analyses myself as I work on another part of the lab.
However, the question is based on how to get the concentration value of the undiluted sample. The standard used have an undiluted concentration of 2123 µg/ml. It is pre-diluted in two steps, first 1/40 and then 1/50 giving a total dilution of 1/2200.
The Standard is then analysed for three different doses 1/20, 1/40 and 1/80. Two times at the beginning of the run, and two times in the end.
The Sample is pre-diluted 1/15 to then be analysed for the same three doses as the standard.
What I have done now is that I used the Parallel Line model to try to calculate the concentration. Unfortunately, I don´t get the same answer as the earlier calculation program (Which is 4,786), and I have been able to figure out is that the problem is that I get a slight shift in the relative potency. Unfortunately, I can´t find where the problem lies.
Hopefully, this clears it up a small bit.

This just doesn't make sense. You say that the undiluted sample has a higher concentration than the undiluted standard. The assay values are of the same order of magnitude for standards and sample. But the standards were prediluted x2200 while the sample was only prediluted x15. If the sample is more concentrated and is prediluted less then it should give much higher readings. Or I don't understand your experiment.

Hi sorry for the late reply. The undiluted standard got a concentration of 2123µg/ml while the sample got a concentration about 4,8 µg/ml.

My answer: 4.79 µg/ml

(All values below are µg/ml)
Calibration data
Determine the mean of the four absorbance values at each dilution.
The calibration curve is then a plot of concentration (x-axis) against mean absorbance. Note that the actual concentration in the assay is (2123/2200)/dilution where dilution is 20, 40 or 80. If you chart this you will see that the data fit well to a straight line.
Use the Excel SLOPE and INTERCEPT functions to derive the parameters of the trendline. (I get SLOPE = 30.59; INTERCEPT = -0.8225)
The equation for converting an observed absorbance value to a concentration is:
concentration = (absorbance - INTERCEPT)/SLOPE
Sample data
For the sample measurements the only one that is valid is that for the 20x dilution because the other absorbances lie outside the range of the calibration data (see note below).
Using 0.406 as the absorbance value in the equation above gives a value of 0.01596 for the concentration in the assay well. This sample was diluted 20-fold for the assay, and the source for that dilution was derived from a 15-fold ‘pre-dilution’ so the original concentration of the sample is 300x the assay value which is 4.788 µg/ml.
Note
I don't know the nature of the discrepancy between your calculations and the target value, but if you try to incorporate the 40x and 80x dilutions for the sample you will get higher values for the sample concentration. Presumably the assay becomes non-linear at low concentrations.

Hi Alan, Thank you´so much for the response. It really helped a lot and I have been able to work out how to perform this when only one of the samples are in range. Now I´m stuck instead on how to incorporate the values when all of them are in range.
Example: Predilution for standard = 1, conc = 1,04
Avg ystd =  1,1585 0,611 0,3205
Y sample = 1,16 0,687 0,345    with a dilution of 30.
I try to put them on a common slope, get a value for the relative potency and then calculate the concentration. The problem is that I get a value of 31,88 when the "correct" result is 33,50.

@Martin    Not sure that I fully understand the numbers you mention, but if you have more than one assay of the sample that is in the range of the standard curve then you can simply use all valid readings to derive separate measurements of the [sample], remembering to vary the dilution factor as appropriate (e.g. x20 above but if the 40x dilution had also been valid then use the same formula but multiply by 600 (15x40) at the last step). You can then take the average value of all of your estimates of [sample]. (Apologies for using 'mean' and 'average' interchangeably here.)

Thank you so much, Alan! Got confused with the common slope that is mentioned in my papers, this helped me out fantastically!


text:
Recommendation for a molecular biology book that explains how we know what we know
My background is in math and I know very little about biology.  The few biology books that I've looked at seem to explain what is known (or what is believed), but don't really explain how we know what is known.  For a specific example, when I hear that "DNA makes RNA and RNA makes protein", I would like to know things like:

How do we know that DNA makes RNA?
How do we know that RNA makes protein?
How do we know that there is such a thing as "protein" in the first place and how do we know what it is?
How do we know that there is such a thing as RNA and how do we know what RNA is?

Can you recommend any books that do a good job of explaining how we know what we know in molecular biology and genetics?

so basically you want a biology textbook and possibly a book about the history of cellular biology. You may want to google Francis Crick and the origins of the "Central Dogma of Molecular Biology" which is will show you how transcription (DNA->RNA) and translation(RNA->protein) were discovered. This slideshare will help you with proteins, https://www.slideshare.net/sabarnisarker/history-of-protein-discovery, The trick isthese are not single discoveries but a series of many many discoveries and experiments building our understanding.

The following wikipedia articles give an overview on the various discoveries that lead to our understanding of genetics. https://en.wikipedia.org/wiki/History_of_molecular_biology
https://en.wikipedia.org/wiki/History_of_RNA_biology
https://en.wikipedia.org/wiki/History_of_genetics

@John Those slides about the history of protein discovery are great, thanks.

@Adrian Thanks, good to know about.  While learning the history of the discoveries can be very enlightening, and might be the best approach for me, I'm not only interested in how it was done historically.  What I would most like to know is, in hindsight, what would be the simplest or most direct way to go about discovering these things.

Just about every molecular biology book that I've seen covers the basics of the history, including providing answers to your questions, via a summary of landmark experiments in the field. I've always fantasized about teaching a "History of Molecular Biology" course, where we read the original papers, but I'm neither employed as a university professor nor confident that others would find that anywhere near as interesting as I would.

This is not my favourite book on molecular biology (Alberts is my favourite, and Lodish is the runner up), but I'd recommend The Cell, A Molecular Approach, by Geoffrey Cooper
This book has, for every chapter, one or more boxes called "Key Experiments", in which the author describes famous experiments that allowed us to know what we know now about that subject.
For instance, at chapter 10, titled "Protein Sorting and Transport", the Key Experiment box shows the discovery of the peptide signal by Gunter Blobel:

And the best news, the book is completely free at NCBI bookshelf:
https://www.ncbi.nlm.nih.gov/books/NBK9839/
It's searchable, but unfortunately not browsable. However, the workaround is very simple: just type the chapter title in the search box!
Of course, some concepts are so old (for instance, you asked "how do we know that there is such a thing as "protein" in the first place") that you probably are not going to find them in molecular biology textbooks, but on a book about history of science instead.
PS: By the way, both Alberts and Lodish are also free to read (and browsable) at NCBI bookshelf!

You may want to try A History of Molecular Biology by Michel Morange, it is currently in its third edition, It will not cover everything (proteins are discovered much earlier), you are asking for a wide swath of biology, but it should get you started.
The Eighth Day of Creation: Makers of the Revolution in Biology is also a good read.  It is also funny to hear Crick bemoan his misuse of the word dogma that has been immortalized by his discoveries, he used it in the title becasue it was "catchy".

Wow a very helpful answer

As a master of science in molecular biology. I would recommend getting the two books.
Biochemistry by Stryer
Molecular Biology of the cell by Alberts et al.
Those two together are the course books used for several semesters worth of molecular biology and biochemistry, covering the central dogma plus quite a lot more. They are very well referenced and are worth every penny.

While I'd agree to some extent (I know them well; we used both at undergrad), I think OP wants a book which actually describes and explains the key experiments in terms understandable to a relative newcomer, rather than simply referencing them.


text:
Reason for specific location of a gnat swarm?
While checking on my yard trees, I noticed a tiny swarm of gnats above one small maple that has a metal cup holder stake used to help train the trunk straighter. Approximate swarm size of 20 - 30 gnats and they hovered about 6 inches above the top of the cup holder.
I know there's studies on the phenomena of swarm behavior, and out of curiosity as to what they would do I put my hand a couple inches above the cup holder. The little swarm repeatedly moved straight upwards 3-4 inches then returned to the original spot as soon as I removed my hand. When I raised my hand up towards the swarm they would move higher and higher and also follow my hand back down as I lowered it. No matter how high I raised my hands if I removed it quickly they returned immediately to the original location. I checked back a half hour later and they are still there and acted the same way.
What might be the reason for that specific preferred location of the swarm? I has been cloudy and humid all morning and I wonder if the metal of the cup holder is changing the air temperature or some other quality that far above itself? I did also notice a stronger sweet smell of the clover in that location but do have clover all over the yard. My other trees, including a very similar sized young maple but without any support next to it, have no swarms so the metal cup holder perhaps is a correlating factor?
I tried adding a picture for reference but can't get it to upload.

'Gnat' is the common name for a number of species of tiny flying insects in the Dipterid suborder Nematocera (https://entomology.ca.uky.edu/ef632), including Ceratopogonidae (biting midges), Chironomid midges (non-biting midges) and Simuliidae (blackflies). Like many other Diptera, a lot of these species mate aerially in swarms: the males gather using visual cues to determine swarm location. I'll try to add more detail to this later on why they go for specific locations, but in the meantime here are some papers on mating swarms in some of the groups normally called 'gnats':
General papers on swarming behaviour in Diptera:

Downes, J. A. 1969. The swarming and mating flight of Diptera. Annu.
Rev. Entomol. 14: 271–298.

Swarming behaviour of the family Ceratopogonidae:

Downes, J. A. 1955. Observations on the swarming flight and mating of
Culicoides (Diptera: Ceratopogonidae). Trans. R. Entomol. Soc. London
106: 213–236.
Campbell, M. M., and Kettle, D. S. 1979. Swarming of Culicoides
brevitarsis Kieffer (Diptera: Ceratopogonidae) with reference to
markers, swarm size, proximity of cattle, and weather. Australian. J.
Zool. 27: 17–30
Zimmerman, R. H., Barker, S. J., and Turner, E. C. 1982. Swarming and
mating behavior of a natural population of Culicoides variipennis
(Diptera: Ceratopogonidae). J. Med. Entomol. 19: 151–156.
Blackwell, A., Mordue, A. J., Young, M. R., and Mordue, W. 1992. The
swarming behavior of the scottish biting midge, Culicoides
impunctatus (Diptera, Ceratopogonidae). Ecol. Entomol. 17: 319–325.

Swarming behaviour of the family Chironomidae:

Gibson, N. H. E. 1945. On the mating swarms of certain Chironomidae
(Diptera). Trans. R. Entomol. Soc. London 95: 263–294.
Oliver, D. R. 1971. Life history of the Chironomidae. Annu. Rev.
Entomol. 16: 211–230.
Fyodorova, M. V., and Azovsky, A. I. 2003. Interactions between
swarming Chironomus annularius (Diptera: Chironomidae) males: role of
acoustic behavior. J. Insect Behav. 16: 295–306.

Swarming behaviour of the family Simuliidae:

Moorhouse, D. E., and Colbo, M. H. 1973. On the swarming of
Austrosimulium pestilens MacKerras and MacKerras (Diptera: Simuliidae). Australian J. Entomol. 12: 127–130
Hunter, D. M. 1979 Swarming, mating and resting behaviour of three species of black fly (Diptera: Simuliidae). Australian J. Entomol. 18: 1–6


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Is monogamy a human innate behaviour?
As the question states, got curious and I was wondering if monogamy is an innate human behaviour or is it because of how we built society (religion, traditions, etc.)?
Let's say we go back in time, would we see humans settling down with a single partner at a time and caring for their children as a couple for life or would they reproduce with several leaving the mothers with their children?
Thanks!

Comments are not for extended discussion; this conversation has been moved to chat.

Please see this meta post for a discussion on why this question was closed.

Not at all... Humans are traditionally a warrior territorial tribal culture, that fight, that catch slaves as trophies, slaves are generally recorded in all human cultures, from roman, greek, north america, south american, papuan, african, oriental, chinese, vikings, slavery was the norm, as soon as the culture was a warrior culture... The female slaves did work for the owners, and they probably weren't nuns!!! I saw a papuan on TV say: my second wife, i ate the husband and buried his leg. the second one, I just ate the brain because i was not hungry and buried the rest. he had 3 wives.

How in the heck is this opinion-based? The are arguments on human monogamousness based on the differences in physiology between humans and other apes (whose sexual behaviour is known, and probably stems from biology rather than cultural expectations). There may be other arguments. Whether someone accepts any of those arguments is different, but then humans are very good at denying things they don't like, regardless of the subject. Even a possible lack of consensus doesn't make something opinion-based: "we don't know for sure but here's what we do know" is a valuable answer too.

@ilkkachu Quickly gain 2899 reputation and vote to reopen!

"leaving the mothers with their children?" I'm a big fan of promiscuity theory, but my question is: where would they leave? Men and women lived closely to each other, in large groups. There was no such thing as a private house.

Humans are believed to be mostly serial monogamists with a noticeable components of secret cheating. Serial monogamy means most will have a single partner at a time but  will likely have several partners throughout their life, there is however an under current (~15%) of hidden cheating in most studied populations. Also I say mostly becasue human behavior is plastic and nearly every possible combination exists, albeit in small numbers.  Males do have a stronger tendency to seek multiple partners at the same time, which makes biological sense.
 like many social species you really have several mating strategies coexisting, often in the same head. Our large brains allow for more flexible approach to strategies.
In other animals exclusive (one mate forever) monogamy is exceptionally, almost breathtakingly rare, (not counting animals that only ever mate once). The Azara's night monkey is one of the few that has been backed by genetic research. Almost every monogamous species ever studied either has some rate of cheating, or is serial monogamous.

Unlike other species humans also have an incredible ability to resist and skew objective studies of their behavior (from reality TV wannabes to lawsuits to crimes against humanity trials) so be mindful of how any such data has been collected.

Data collected from the Ache hunter gatherer tribe suggests that humans were somewhat promiscuous even when it could not be kept hidden. Relative testes size, which for humans are intermediate between highly promiscuous chimpanzees and the gorillas with their single sire harems, would tend to confirm an intermediate level of promiscuity.  The Ache data suggest that a moderate level of promiscuity was adaptive, with survival to adulthood maximized at about two potential fathers per child due to the significant chance of fathers dying from violence before their children reached adulthood.

Answer would be improved by contextualising monogamy with an example of a species that is actually monogamous.  I remember seeing a documentary which mentioned a species of lizard which pair for life, and walk side by side for the rest of their lives until one dies.  But maybe it was just a dream I had when I fell asleep watching a nature program... point is, we often think we're "monogamous" but biologically speaking there are many species which actually pair for life and put our romantic efforts to shame.

I claim that humans have only one partner at a time only because they are too lazy to prove others that they do not live wrong if they choose to have several partners at once. Unless a date lasted for a few hours in prehistoric times.

The easy answer is simply, no.
The longer answer is that it depends on whatever cultural norms that are practiced in a given area at a certain time.
Often powerful men in history had multiple lovers, but had arranged marriages. Like wise open relationships were very normal in the 60's and 70's of the 20th century. Also polygamous relationships are practiced in certain religions today.
While in modern times, especially in the west, we seem to tend toward the monogamous relationships, it seems to be more dependent on culture rather than biology.

As a personal comment. If we were evolved to be monogamous it seems rather conflicting that we can be sexually attracted to other people besides our current partner.

Mating partners die sometimes, and quite frequently in the past. Bonding so strongly that you don't find another attractive makes no sense.

@fredsbend: But many, if not most, humans actually act on those attractions without waiting for the death of the current partner.

@James 1) That has nothing to do with the original assertion in Jeppe's comment. 2) "Many" and "most" are not words I'd use to describe 15% of the population.

@fredsbend my original comment was mostly focused on the cases were sexual attraction occur despite the partner being within a few meters. However if that increases the chance of passing on our genes, it is hardly surprising that we feel that way. From a simplified perspective; males being opportunistic while females seek stability and safety, would make good sense based on the hunter/gatherer theory. Males would then seek to pass on their genes as often as possible, while females would prioritize the safety of children by pursuing relationships with the males supplying food most often.

"males being opportunistic while females seek stability and safety". I think that's the leading theory to give explanatory power to male/female interactions.

@fredsbend: True, but the problem is not with the many/most observation, but with your 15% statistic.

@Jeppe Nielsen: You do realize, don't you, that a good many of us engage in sex without any intention of passing on our genes?  Indeed, some of us spend time & money to avoid doing so.  Over $19 billon in the US, as of 2015, per this: https://www.gminsights.com/industry-analysis/contraceptives-market-report

@jamesqf, most certainly... but do you realise how few generations that have had that option. Also, sex in other species can be used in to build social cohesion. So sex doesn't have to be about having children.

@Jeppe Nielsen: I think it's always been an option (at least since humans recognized the connection between sex and procreation), it's just that current technology makes it much more convenient.  There are records of birth control techniques as far back as 1500 BCE: https://en.wikipedia.org/wiki/History_of_birth_control

And as horrible as it sounds, abandonment has been a common method for a long time. Birth the baby, leave it somewhere.

@fredsbend 15% is definitely many people. Many enough to take them into account and explain their existence more argumentatively than "They exist only due to random useless mutations". Also, an average polyamorous human might be much more attractive/fertile than monogamous. This is another important factor. There is literally no sense in a completely unattractive person wanting to have multiple partners because it is insanely hard to get even one.

@JeppeNielsen That theory is flawed. Males do not seek as much partners as they can, otherwise they would be attracted to any female they see. Why so? Because societies where everyone had almost equal amount of offsprings could be better suited to survival than those where most offsprings belong to one or a few males. For a further support males wanting to have several partners are not often competitive. Also, females would not be only ones being interested to save their children, because if you pass genes to 100 females and all your children die you are less fit than an average male.

@jamesqf To pass your genes you don't actually need to have an intention of doing exactly that. Especially when there is no contraception. Most animals don't have a desire to become a parent.

I just read a book on the Evolution of Sex and  one of the questions was why primates have lost the estrous cycle. The thought was that the sexual desire of the female anytime rather then periodically tends to keep the male "at Home" ensuring survival of the female and offspring. This implies that males are genetically engineered for monogamy but since females can survive now without a male (as opposed to those living in a cave) some males at least in younger years practice polygamy as do females.

No, they are not.
Polygyny, polyandry and group marriage are, or have been, practiced in various cultures. Polyamory and other forms of non-monogamy are practiced. There are estimates that four to five percent of Americans are involved in consensual non-monogamy (despite social pressure for monogamy).
A sizeable portion of what the porn industry is creating revolves around the subject of threesomes, group sex, cheating, cuckoldry etc. etc., so quite apparently there is a market for that. It turns people on, be that for the thrill of "breaking the taboo" or some underlying desire. (Excuse me for not posting a link to back this up. Use your favourite bookmark.)
There is nothing to indicate that non-monogamy in any of its forms is "unnatural" to humans. Tabooed in some cultures and / or religions, but not unnatural.

...over much of human prehistory, polygyny was the rule rather than the
  exception...

Dupanloup I, Pereira L, Bertorelle G, Calafell F, Prata MJ, Amorim A, Barbujani G (2003). "A recent shift from polygyny to monogamy in humans is suggested by the analysis of worldwide Y-chromosome diversity". J Mol Evol. 57 (1): 85–97 (quote from p. 94)

This paper puts that shift at about 18,000ya -- roughly the same time that agriculture became common, but much too recent to claim that Homo Sapiens as a species is now "naturally" monogamous.
It is rather something that developed culturally:

...an analysis of foragers in the Standard Cross-Cultural Sample reveals that male provisioning does affect the mating system. Societies with higher male contribution to subsistence are more monogamous.

Frank W. Marlowe. "The Mating System of Foragers in the Standard Cross-Cultural Sample". Cross-Cultural Research, Vol. 37 No. 3, August 2003 282-306 (quote from the abstract)

On page 147 of "The myth of monogamy. Fidelity and infidelity in animals and people" (ISBN 0-7167-4004-4), David P. Barash concludes that about 80% of human societies lived polygynous before they came into contact with the "Western" culture.

The question is about a general characterization of the species. You've posted examples of exceptions, not generalizations. That's cherry picking, a logical fallacy.

@fredsbend: At which percentage of current population living non-monogamous, or historic records of non-monogamy, do these so-called "exceptions" suffice in your eyes to indicate that we as a species are not "naturally" monogamous? It's a cultural / religious taboo, mostly.

@fredsbend: FWIW, lifting from WP, three representative studies in the USA found that "about 10–15% of women and 20–25% of men engage in extramarital sex". There are more numbers in there. That's a pretty large number of "exceptions" to uphold a claim that humans were "naturally" a monogamous species. (Be very aware when crossing the line where you're calling non-monogamous people "unnatural".)

"It's a cultural / religious taboo, mostly." *citation needed

A taboo shared among cultures and religions throughout millennia. I don't think the evidence can suggest religion and cultural taboo is the only reason people are monogamous. Instead, the fact that it's a widespread taboo suggests something bigger. Something like "innate behavior", or simply "biology".

Don't put a value judgement on the word "natural". The plain meaning is "existing by nature". As the top (and correct) answer says "Monogamous, plus a small minority of cheaters" is an appropriate characterization. Your answer, "no, not monogamous", is not just a mischaracterization, but wrong.

@DevSolar: I think your numbers don't include what seems to be a very large majority of Americans/Western Europeans who engage in sex (often with multiple partners during the same time span), before marriage or in the intervals between marriages.  So maybe most are serial monogamists if you compress "serial" down to a day or so :-)

@fredsbend: I take "natural"/"innate" behaviour to mean "freak cases nonwithstanding". Tigers are natural carnivores. Horses are natural flight animals. Swans are naturally monogamous. Humans sometimes are, sometimes aren't monogamous, so saying they are "naturally" so is just false, and marginalizing a sizeable portion of the population. Also, you seem to confuse this with a discussion forum. Post a dissenting answer and downvote mine, if you like, but I woukd wellcome if you could get off my back about this.

@James That's a good point. But what is the actual incidence of  people who "sleep around before marriage"? Yes, there's a hookup culture, but my impression is that most people aren't having multiple sex partners day-to-day, month-to-month, or even year-to-year.

@fredsbend: You're still confusing "mainstream culture" with "natural / innate" behaviour.

@DevSolar Nope. I concede a "hookup culture" which may be an indication of a natural behavior, but then immediately challenge that notion. "Yes, [concede a point], but [challenge the implication]" is a common form and does not indicate confusion on the point or the implication. In fact, it demonstrates the opposite. I thought you wanted me to leave you alone?

@fredsbend: These are the comments to my answer you're confusing with a chatroom, and I get notified when you post. And I challenged your closing statement, because it is assuming Western culture as "what's innate behaviour". Check the updates to the answer. Comments are for improving an answer, not discussing an alternative viewpoint or trying to change the poster's mind.

Why do you keep pinging me? I've been using SE for 5 years. I know the rules on comments and I don't think I've done anything out of the ordinary here.

Consequently, your edited answer is certainly better than the original. Down vote removed. However, I think you need a source for "18000ya [is] much too recent to claim that Homo Sapiens as a species is now "naturally" monogamous." But the Barash source is provocative. I'll be looking closer at that one.

@fredsbend: If humans were "naturally" monogamous, the first person anyone has sex with would be the only one (barring death &c)  (Like some fish, where the male embeds himself in the female.)  But (per CDC statistics: https://www.cdc.gov/nchs/nsfg/key_statistics/n.htm ) the average is 4-6.   When you consider that many people either don't have the practical option of having multiple, frequent sex partners, or choose not to do so for religious/cultural reasons, the conclusion is that the majority aren't monogamous by nature.

@James Yeah, I didn't want to get into the definitions of monogamy, but that seems inevitable. Monogamy certainly can mean one mate for life, but another definition is one mate at a time. Then we have to define mate too. I would take the definition that it has more to do with procreation and less to do with sex. Ugh. I'm starting to not care.

@fredsbend: S. Fink, L. Excoffier, G. Heckel: Mammalian monogamy is not controlled by a single gene. In: Proceedings of the National Academy of Sciences of the United States. 103, Nr. 29, March 2006, S. 10956–10960. I think you will agree that 18kya is a bit on the short side to make Homo Sapiens come about full swing on a multi-gene trait...

@fredsbend: WRT monogamy as "one mate at a time", how short a time are we looking at?  Years, months, weeks, days?  Certainly when we get down to minutes, there are fairly obvious physical limitations :-)  Defining "mate" as procreational rather than recreational has difficulties, too.  There are people who choose not to procreate but who enjoy recreational sex; there are likewise half-siblings are by no means vanishingly rare.

@James I don't want to comment much further on this (maybe I would in chat). You bring up some good points, but among many of them we could flip the challenge that has been put on monogamy. The non-monogamous behaviors could very well be culturally influenced more than biologically, and it could be that monogamy is more biologically influenced than culturally.

I wouldn't call humanity polygynous as well. As you said: "group sex, cheating, cuckoldry etc. etc." This quite disproves this theory. As well as that many people (including men) do not have jealousy. I only suspect that many others are jealous because they are only complying to rules (like getting angry if you go to a theatre in shorts) which are not natural. Probably, we are the only primates with group sex (in particular gang bang) and that might explain our differences from other polygynandrous/with dispersed mating primates (like solid ejaculates, dimorphism and big testes).


text:
How do I know which molecular structure is glycine's "base state"?
I was looking up the chemical structure of glycine, and I found the following two images:
and
.
My question is, what is the "base state", or the "natural state" of glycine? Under what scenarios does glycine become oxidized/reduced?
Also, I know that amino acids contain a carboxyl group, an amino group, a lone hydrogen atom, and a side chain. What is the formula for the amino group? Is it $\ce{-NH_2}$ or $\ce{-NH_3^+}$?

Both are correct, both are the natural state of glycine and both represent the base state. Amino acids are zwitterions, which switch freely between the two states. Try googling zwitterions.

So, they are just different ways of representing the same thing? Is there a "more correct" diagram?

edited my first comment, try searching for zwitterions.

If you want to be really specific the forms exist in equilibriums, but may be affected by pH. if the ph I very low, glycine is positively charged, neutrally charged around average pK value for the amine and carboxylic acid groups, while negatively charged at high pH.

Wait, so the amino group can be represented as either NH2 or NH3+?

Correct, both are entirely correct. However at physiological pH (6-8), typically the zwitterform with charges are used.

For the sake of completeness: the second molecule should have a negative charge at the -COO group

I really think this should be closed. The poster does not define his question properly — there is no such thing as base state — cannot copy the correct structure of the zwitterion form, and is ultimately asking the most basic of questions the answer to which can be found in any text or web resource. In addition it is ultimately chemistry rather than biology.

Please note that these are acid/base reactions and not oxidation/reduction reactions. If glycine is oxided or reduced its not glycine anymore.

Short Answer: You need to define base state.
Background: The point to keep in mind here is that the base state (as you call it) is not constant. As @jeppenielsen points out in the comments, amino acids are zwitterions. According to Wikipedia:

In chemistry, a zwitterion, formerly called a dipolar ion, is a neutral molecule with both positive and negative electrical charges. (In some cases multiple positive and negative charges may be present.) Zwitterions are sometimes called inner salts. Unlike simple amphoteric compounds that may only form either a cationic or anionic species, a zwitterion simultaneously has both ionic states.

In glycine, the center of positive charge is the -NH2 group while the center of negative charge is the -COOH group. At different pH (acidic, neutral or basic), the structure of the molecule keeps on changing as shown in the image below:
source
Structure of other amino acids also changes similarly. To know why this change occurs, just keep in mind that (in very simple terms) pH is inversely proportional to the concentration of H+ ions in a solution (higher the pH, lower the concentration of H+). The exact formula is $\ce{pH = - log[H_3O^+]}$ (yes, it means that a pH of 4 is 10 times more acidic than pH 5 and so on). Also, as pH changes, so does the formula for the amino group (see the diagram again).

Good answer, as always, but this is incorrect: "keep in mind that pH is inversely proportional to the concentration of H+ ions". The bigger the pH the lower the H+ ions concentration, that's correct... However, inversely proportional has another meaning in math: it means that the multiplication of the two variables is a constant. And that is clearly not the case here, do the math and you'll see. Actually, you can have a variable growing while the other one decreases and still they can be directly proportional!

That was a simplification, thats why I also put the formula with it. But I'll change it if it seems incorrect :) seems better now?

Kind of. Just say that "the higher the pH the lower the H+ concentration".

or say pH=-log(H+) and do it correctly. ah I see it was added alredy.

@jeppenielsen thanks! There is a post on chemistry.SE (whose link I am unable to find right now) which discusses about why it is better to write $\ce{H_3O^+}$ instead of $\ce{H^+}$ :)

H3O+ only works if you use water as solvent... you could use ammonia as a solvent and H+ would still work. Or you could be in a nonpolar solvent. H+ only fails in heavy water, but then we should be writing pD instead anyways

@jeppenielsen since we're talking about it in biological perspective, we can assume water to be the solvent ;)

Not in the lipid bilayer of the cellmembranes.

@jeppenielsen Do you expect free (polar/charged) glycine to be found in the (hydrophobic) cell membrane? I don't...

Only in extremely low concentration.  But using pH=-log([H3O+]) instead of [H+] is silly especially since we have general notaion for all solvents. Also [H+] is significantly different than [H3O+] in some cases.

Thats why I was talking about that chemistry.SE post. It clearly talks about why we use H3O+ instead of H+. In short, H+ is too unstable to exist and readily reacts with any nearby molecule. Mostly it forms H3O+, but it can also form H5O2+, H7O3+ and even H9O4+. So, once you know what is actually happening at the concerned scale, writing H+ becomes a lot more silly.


text:
Do proteins generally contain phosphorus and sulfur?
I've heard that proteins generally contain six main elements - carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur.
I know that proteins are made from amino acids. Amino acids are composed of an amino group, a carboxyl group, a lone hydrogen atom, and a side chain that varies between amino acids. Of the 20 major amino acids, none of them have a side chain that contains phosphorus. Only cysteine and methionine contain sulfur.
So, are sulfur and phosphorus atoms really characteristic in the structure of a protein?

Well, phosphorus is only present in some proteins which are subject to post translational modifications, such as phosphorylation. Sulphur can originate from either cystein or methionine present in the protein. So only proteins that are modified after translation will contain phosphorus.

So, phosphorus is not characteristic in the structure of a protein, right?

Both phosphorus and sulfur are important to the functional structure of many proteins, even if phosphorylation happens later.

Bryan that is wrong, show me a source on that please. As the asker points out, phosphorus is not present in the amino acids which make up the protein. The phosphor present will have been added after translation by the ribosome, thus as post translational modifications. PTMs typically occur after folding. That phosphorylation occurs is true, but it is usually not essential for protein structures, unless it changes the conformation of the protein significantly.

@JeppeNielsen "Bryan that is wrong" - your own comment contradicts that: "unless it changes the conformation of the protein significantly" - this is precisely what I mean. And many proteins are constituitively phosphorylated at certain residues, rather than the impression that new biology students get (like the people often asking questions here) that phosphorylation is usually a sort of on/off switch. That was my point.

And for how many proteins have it been proven that phosphorylations are essential for stability.

@JeppeNielsen I don't think you understand what he is saying.

@JeppeNielsen I didn't mention stability, though phosphorylation state can be a marker for degradation (the tau protein is an example). In terms of structure, one example mechanism is that some proteins are only functional in a dimerized form, formation of which can depend on phosphorylation. Phosphorylation completely changes the chemical properties of the modified residue. Base substitution is sometimes used experimentally to approximate "permanently phosphorylated" residues, which suggests that phosphorylation is of similar importance to base substitition in structure.

Of the 22 known proteinogenic amino acids, all contain hydrogen, carbon, nitrogen and oxygen. Some (methionine and cysteine) contain sulfur while one (selenocysteine) contains selenium. None contain phosphorus, but this element can be incorporated by:

Post translational phosphorylation of various residues. This often allows/prevents binding of other proteins and/or triggers a conformational change in the target protein. It is also necessary for proper folding of some proteins (example). Sulfur can also be incorporated in a similar manner (sulfation).

Incorporation of phosphorus containing prosthetic groups. This can occur covalently and is necessary for the function of some proteins. Sulfur can also be incorporated as part of prosthetic groups.

You may also consider the other elements necessary for the structure/function of many proteins: iodine in thyroglobulin, iron in hemoglobin, etc...


text:
How many primary oocytes in human female body at birth?
https://discovery.lifemapsc.com/library/review-of-medical-embryology/chapter-4-gametogenesis-oogenesis
In the above site, I see that:

About 2 million primary oocytes are found in the ovaries of a newborn
  femal Many regress during childhood so that at puberty about 30-40
  thousand remain. Only about 200-400 of these ever reach full maturity
  after puberty and are expelled at ovulation during the female's
  reproductive life

http://www.pnas.org/content/107/22/10280.full
Also, from this site, I see that

Human ovaries contain follicles as basic functional units. The total
  number of follicles is determined early in life, and follicle
  depletion leads to reproductive senescence. Human follicles begin
  development during the fourth month of fetal life, and each human
  ovary contains ≈400,000 follicles at birth.

From my understanding, there is one oocyte inside one follicle. So, two number should be the same. Why there is a big difference? Or my understanding is just wrong?
PS. I am doing research for my sci-fi, I didn't learn this topic in any college, sorry if this is a silly question.

keep in mind the body is capable of generating new oocytes and follicles, https://link.springer.com/article/10.1385/ENDO:26:3:301

@John definitely read about it in source 3 of the answer.

Short answer: The developmental process starts from oogonia as follows:

Oogonia(7million) in the foetus develops into primary oocyte(2million) in the foetus prior to gestation which again develops into primordial follicle(700,000-800,000)at birth.

From the second excerpt of your question I could understand that it said, "each ovary contains  approx. 400,000 follicles at birth." which is definitely correct if you consider that total number of follicles in both the ovaries would give 800,000.

Excerpts from the references that lead to the short answer above:

In the developing female fetus, oogonia become primary oocytes that begin the first division of meiosis. However, this division is not completed and the primary oocytes remain “frozen” in the prophase stage of the first meiotic division.
At birth, oogonia are no longer present. Each primary oocyte is surrounded by a single layer of squamous epithelial cells called follicular cells. The primary oocyte together with its follicular cells is called a primordial follicle. There are about two million primordial follicles with their primary oocytes in the ovaries at birth suspended in the first division of meiosis.
As the female grows, primary oocytes begin to die and disappear with their follicular cells. This process continues until puberty when there are only about 400,000 primordial follicles left in the ovaries. The primary oocytes continue the process of oogenesis after puberty begins.[Source]

The total number of primary oocytes at birth is estimated to vary from 700,000 to2 million. During childhood most oocytes become atretic; only approximately400,000 are present by the beginning of puberty, and fewer than 500 will be ovulated.[Source]

Primary oocytes reach their maximum development at ~20[6] weeks of gestational age, when approximately seven million primary oocytes have been created; however, at birth, this number has already been reduced to approximately 1-2 million.Recently, however, two publications have challenged the belief that a finite number of oocytes are set around the time of birth.[Source]

In the human embryo, the thousand or so oogonia divide rapidly from the second to the seventh month of gestation to form roughly 7 million germ cells.[Source]

REFERENCES:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0008772

"There are about two million primordial follicles with their primary oocytes in the ovaries at birth suspended in the first division of meiosis." doesn't this imply that there are 2Million follicles at birth, which clearly contradicts the information provided by OP?

@JM97 I want u to read source 2.that will answer ur question...

then add this point of source 2 :  "The
total number of primary oocytes at birth is estimated to vary from 700,000 to
2 million", could you provide any research paper/ or something more credible for that statement in second source? It would be much helpful.

Thank you @JM97 You make this question active again. lol


text:
Which mRNAs enter P-bodies?
Processing bodies (P-bodies) are distinct foci within the cytoplasm of the eukaryotic cell consisting of many enzymes involved in mRNA turnover (ref). They play a fundamental role in RNA silencing/interference, particularly as an antiviral response, since they are the key site for siRNA-bound RISCs (small interfering RNA-bound RNA-induced silencing complexes) to degrade mRNA with an exogenous origin. Some mRNAs entering P-bodies then leave and re-initiate translation, and the switching mechanism for this is currently poorly understood.
However, I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation. Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?
It seems rather odd if RNAi has evolved to give viruses two independent targets for evasion, but if the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated (and therefore postpone movement to the P-body)? I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.
The paper cited above says "The available evidence indicates that P bodies are sites where mRNAs that are not being translated accumulate, the information carried by associated proteins and regulatory RNAs is integrated, and their fate — either translation, silencing or decay — is decided", but this is from 2007 and I'm aware RNAi is a very fast-moving field.

I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.
To be clear, P-bodies are in the cytoplasm (ie they are not separated by a membrane). There is also dynamic exchange of components between the ribonucleoprotein complex and free cytoplasmic pool (1):

Most P-body components are distributed diffusely throughout the cytoplasm as well as being localized in P bodies. Quantitative information regarding the fractionation of these proteins between the cytoplasm and P bodies is still lacking, but given the volume of P bodies relative to that of the cytoplasm, the diffuse cytoplasmic fraction could be significantly larger, although the concentration of mRNA-decay factors might be much higher in P bodies. Also, P-body components dynamically exchange with the cytoplasmic pool, which indicates that decay enzymes and co-activators are not confined to P bodies. So, it is probable that mRNA decay also occurs, and might even be initiated, in the diffuse cytoplasm, and that P bodies arise by association of mRNA-decay intermediates induced by interactions between decay enzymes and cofactors. The concentration of mRNA-decay intermediates and mRNA-decay enzymes in P bodies would be expected to increase the speed of degradation and, in turn, reduce any potential competition between these RNA fragments and normal mRNAs for limiting cellular proteins involved in mRNA regulation.

I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation.
mRNA can also be degraded by exosomes (1):

In eukaryotic cells, degradation of bulk mRNA occurs by two alternative pathways, both of which are preceded by removal of the poly(A) tail by deadenylases. Following this first rate-limiting step, mRNAs can undergo 3'→5' exonucleolytic decay, which is catalysed by the exosome... Alternatively, after deadenylation, the cap structure is removed by the decapping enzyme DCP2, rendering the mRNA susceptible to 5'→3' digestion by XRN1 [a P-body associated protein].

Also see (2), and this image therein:

If the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated?
That is, in fact, not the requirement (3)

Recruitment of mRNA to PBs is not an occurrence of non-translation, rather requires active silencing via miRNA or RNAi mechanisms.

They reference another paper (4):

Recent studies with mammalian cells have shown that P-body integrity is not required for ARE-mediated mRNA decay or silencing mediated by fully or partially complementary exogenous, transfected small interfering RNAs (siRNAs). In this study, we investigated the requirement for P-body integrity in NMD, mRNA decay, and silencing mediated by miRNAs and long double-stranded RNAs (dsRNAs). We show that these pathways are unaffected in cells lacking detectable, wild-type P bodies. However, although P bodies are not required for silencing, active silencing pathways are required for P-body formation in Drosophila melanogaster cells, indicating that P bodies are not the cause but a consequence of silencing.

Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?
The RISC complex can be involved in initial recognition and cleavage of viral RNA and the resulting fragments are subsequently degraded by the exosome or P-body associated proteins. RNAi associated components have been observed to be localised with P-bodies (1):

Endonucleolytic cleavage of siRNA or plant miRNA targets is catalysed by the C-terminal PIWI domain of Argonaute proteins... Following this endonucleolytic cleavage, the resulting mRNA fragments are handed over to the general mRNA-decay machinery. In D. melanogaster, 5' and 3' mRNA fragments that are generated by Argonaute-mediated endonucleolytic cleavage are degraded by the exosome... and by XRN1, respectively.

You can also consider the R-gene viral defence mechanism in plants which induces P-body formation and suppression of translation in an RNAi independent manner (5):

Plant NB-LRR proteins [R-genes] confer resistance to multiple pathogens, including viruses. Although the recognition of viruses by NB-LRR proteins is highly specific, previous studies have suggested that NB-LRR activation results in a response that targets all viruses in the infected cell... NB-LRR signaling does not result in the degradation of viral transcripts, but rather prevents them from associating with ribosomes and translating their genetic material. This indicates that defense against viruses involves the repression of viral RNA translation... As a consequence..., NB-LRR responses induce a dramatic increase in the biogenesis of RNA processing bodies (PBs). We demonstrate that other pathways that induce translational repression, such as UV irradiation and RNAi, also induce PBs. However, by investigating the phosphorylation status of eIF2α and by using suppressors of RNAi we show that the mechanisms leading to PB induction by NB-LRR signaling are different from these stimuli, thus defining a distinct type of translational control and anti-viral mechanism in plants.

There are many articles discussing how viruses subvert and/or repurpose P-body mediated decay if you want some further reading (3), (6), (7).

Wow - very comprehensive, thank you very much! I suppose I should leave the bounty unawarded for a couple of days in case someone's preparing something even more impressive, but I can't really see that happening.

@arboviral You're welcome! Yes leave the bounty; let's hope someone adds more information.


text:
What is this strange worm-like creature?

Hi! While I was in my front yard this morning, I happened to look down and see this little guy wiggling thru the grass. He isn't like anything I've seen before.
He is about 2 1/2 inches long. He has a small horn coming out of his back near what appears to be his behind. His belly is a light green color. Also, he starts to flick around when I touch him (To catch him, I scooped him up in a small pot.)
I live in north west Mississippi in the hills near the delta. I am also surrounded by a large forest with all kinds of both pine and normal trees, if it helps.
Thank you in advance!

A picture of the underside or a profile would probably be nice if you still have it around. Most likely a caterpillar or another larva. A giveaway that it is an insect larva is if you inspect the legs, you will see that there are 3 pairs of true legs, near the head, and any other leglike things along the rest of the segments of the body aren't really true legs.

Sorry, but I put it back where it was little while ago!

Also, it had really stubby legs, if that helps.

The horn on the last segment is caterpillar-like. "stubby legs" too. Searching for "caterpillar with horn" led me to species of this genus: https://en.wikipedia.org/wiki/Manduca, but the photos of caterpillars I got didn't look like yours. The colour of yours is not a familiar caterpillar colour for me.

I believe this is some sort of Cranefly larvae, see here:  I've found these guys both directly in streams and along the banks of rivers, but also underneath rocks far away from major sources of water. There are different types of cranefly larvae, but they all have the same characteristics, (bulbous bodies, worm like, not easily noticeable arms, alien encephilization)

It may also be deer fly larvae ( a type of horsefly ) but they typically are more "spiky" on the sides.


text:
Do different chiral centers on ligands cause different confirmational changes and effects in their target proteins?
Say pathogenic bacteriaA makes toxinA, which had D-amino acids instead of L-amino aids, does this difference in chirality cause a different conformational change in the receptor or enzyme, thus leading to either deactivation of the enzyme or signal transduction pathway or activation of a different pathway?
I understand what chirality is in the concept of organic chemistry — rotating plane polarized light, ingold-prelog system etc; however I never leaned what structural feature of chiral molecules changes the way they react inside a cell.
I do NOT understand HOW changes in chirality can be associated with cellular toxicity.
links:
https://www.ncbi.nlm.nih.gov/pubmed/24752840
http://www.jomb.org/uploadfile/2014/0113/20140113053743849.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960212/

There a few things you have to take care of with chirality in biological systems:
First note, that for amino acids we usually use L and D instead of r and s nomencalture.
In chemistry the difference between chiral enantionemeres is usually really just a difference in light polarisation like you described, otherwise they can be thought of as identical, since they have identical chemical properties. This way of thinking does not apply to biochemistry - the moment enzymes (large molecules with very defined 3D structures) are involved the structural difference between the two forms becomes very important for each and every biological reaction.
In the case of single amino acids this means that D amino acids are toxic to eukaryotic cells, because their similarity to the D form allows them to interact with some of the enzymes that usually bind it, but the binding is not a perfect match so the enzymes get inhibited, which makes the D form toxic. (This is already described in the second paper you linked:)

In animal studies, administration of D-amino acids to rats and chicks resulted in growth inhibition [18]. In addition, serious damages such as suppression of the synthesis of glutamate oxaloacetate transaminase, glutamic pyruvic transaminase, and lactate dehydrogenase resulted from D-amino acids accumulation in animal tissues [18].

Now in your question you are asking about the difference between a toxin made from the 'wrong' amino acid. The thing is, this change of the protein will most likely mean, that its not a toxin anymore. A protein toxin is toxic because it can interact with other proteins, based on its 3D structure. This structure is based on the chemical and structural properties of the amino acids building it. If you change the underlying structure of every amino acid it will fold differently and you will get completely different protein - and not a mirrored version of the original protein/toxin.

No.
One can make no generalization about the effect of the change in chirality in a ligand in the protein to which it normally binds. As the simple diagram below shows, as far as interaction with the ligand binding site is concerned there is no essential difference between a enantiomer of the normal ligand and a modified version of it:

Both may be able to interact with sites ‘a’ and ‘b’ on the protein, but whether this will be inhibitory or not cannot be predicted — it will depend on the energy of the interaction compared with that of the correct interaction (and the relative concentrations of substrate and inhibitor).
If it does bind it is most unlikely to cause a conformation change, and even less likely to trigger an alternative pathway. Most protein binding sites are tailored for a single response. In the event of disruption, inhibition is the most likely result.
As far as a bacterial toxin is concerned, the fact that it may employ D-amino acids is a red-herring. The overall structure of the toxin is what counts, and has evolved to act on a specific target. Each example is likely to be unique.
Any textbook of biochemistry will have sections on the substrate specificity of enzymes (e.g. Berg et al. online).

As Nicolai has mentioned in his answer, change of chirality (L and D) of amino acids will drastically change the way a protein folds. I searched online to find if a solved structure of D only form of any protein. However, there were none.
But, both right handed and left handed DNA are known. This difference does not happen because of the chirality difference of the DNA constituents but the way the bases are base paired. However, it exemplifies how the change in chirality can lead to non-trivial change in structure.

Original uploader was Richard Wheeler (Zephyris) at en.wikipedia - Originally from en.wikipedia; description page is/was here., GFDL, https://commons.wikimedia.org/w/index.php?curid=2117121
I will read some more on signal transduction and return to the question.


text:
What are these shrimp-like insects in my cat's water bowl that appear overnight
Our family has 2 cats and a dog.  We keep food and water bowls outside for them.  We clean and refill the water bowls every day.  Almost every morning, the water bowl is teeming with small aquatic insects of some kind, which look and act like little shrimp.  I would guess them to be 5 to 8 mm in length, on average.
What are these, and where are they coming from?  They appear to be aquatic, since they survive and swim in the water for hours -- but how do they get there?
We live in central Florida, USA.

They are not fleas are they?

No, much larger than fleas.  I would guess them to be 5 to 8 mm in length.  I'll add that to the question.

After more research, my leading theory is that these are springtails.  Springtails are water-loving.  They come in linear and globular forms, and these seem to match pictures I've seen of the linear form.  The globular form look more like a spider.  If anyone can confirm this identification, that would be great!

I live in south west Florida and found them in my dogs water bowl this morning! I’ve had saltwater aquariums for years and I am very familiar with these. They are definitely amphipods. I am in shock though as I can’t imagine where they came from. We are not close to the beach and I haven’t had my aquarium set up since I lost it in hurricane Irma in September. So weird. They must be around in the back yard around my banana trees or something.

They are probably some species of amphipod.
According to that link, two species common to Florida are Talitroides topitotum and Talitroides allaudi, though there are dozens of species in the US alone. In some areas, amphipods may be known commonly as "scuds."
These guys like to live in fairly wet places, depending on species - on the beach, in decomposing mulch/leaf litter/grass. They seem to be finicky with moisture: they tend to seek drier areas when it rains, often bringing them onto sidewalks or indoors, then they get dry and look for moisture. I'm guessing this is how they end up in your cat bowl: you certainly are not the first one to observe this.
https://www.whatsthatbug.com/2004/11/10/lawn-shrimp-3/

I'm not sure at all about the precise species...the species most commonly encountered by people on the sidewalks and such don't seem like they would survive long truly immersed in water since they avoid rain, but I wasn't able to find anything definitive on that - maybe their behavior is to avoid very wet but they can still survive immersed for awhile.


text:
I can't see anything at all in my microscope
I just got the Amscope M102C microscope, and it is the first microscope I've operated. I decided to try to look at a fly leg at 40x magnification, but all I could see were the blobs in your eye you get from looking at something bright, as well as a few dots that appear to be on the lens. I tried focusing, cleaning (even though it was fresh out of its package), but I still couldn't see anything. It's so blurry I can't even make out any shapes. Could I please have some help?

40X is almost certainly an immersion objective, this type of objective isn't meant for looking at things like fly legs, it is meant for looking at tissues and cells. You are probably looking for a dissecting microscope. Hopefully your microscope came with some instructions.

Any 40X objective I've used is not an immersion lens. Furthermore, 40X magnification implies 4X objective and 10X ocular. But, yes, a dissecting microscope should be used for this application. Compound microscopes are not ideal for looking at thick, 3D objects.

Understood, but I've also observed (or tried to) onion skin, blades of grass, and a strand of hair and there would be no way of telling there was even anything under the microscope at all.

There are YouTube videos that will take you step-by-step through the process.

@BryanKrause All the 'students microscope' we used at college and university, contained a 40X or 45X objective  not to use with oil. Just like the 10X objective.

@canadianer Right you are - when I read the post at first I read it as the 40x objective rather than the full magnification. My mistake.

@canadianer err same mistake :P


text:
Is this a flowering plant?
I just received a small plant as a gift from a friend.

Here is its leaf:

I tried looking it up on flowers of India, but their database is too much to read manually.
Physical description:
It's short, around 5 inches, probably a flowering plant as per my experience (She says it is a cactus but I don't think so). The leaf is around 1.5 cm and has a cone+cylinder like structure.
Which species is this plant, and is it a flowering one?

Any help would be great.

It's a Crassulaceae.

@GerardoFurtado Thanks, could you please write it as an answer.

Thanks, ABcDexter, but I'll decline your offer. There are too many species, not to mention hybrids and cultivars. If I just write "this is a Crassulaceae", I'll get a bunch of downvotes. Let's wait more time, maybe someone identifies the species. By the way, I forgot to say: the answer to your question is yes, this is a flowering plant, crassulaceans are angiosperms.

Thanks again @GerardoFurtado. Could you check if this is the one Pachyphytum viride

It looks like, but this is a very complicated group.

Crassula tetragona, also known as mini pine tree (for its extreme use in bonsai technique), native to South Africa.

It is a succulent; a xerophyte (a kind of plant which needs very less water for survival), characterised with fleshy leaves developed due to evolution for storing water, this plant attains a height up to 3 meters.

Flowering in this plant usually take place in summer season, the flowers are yellowish orange and white.

Please edit your answer to add discussion of key features that led you to this conclusion and supporting references — i.e. what makes you certain this is Crassula tetragona rather than some other Crassula (or a hybrid as mentioned by @user24284). Without this a non-expert cannot evaluate whether your answer is correct. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

This seems to be of the very variable species of Cotyledon orbiculata. Probably the flanaganii variation.
If that proves to be right, your plant is very much flowering. Since it is native to south africa, I don't know if you will be able to witness its flowers in your home or garden.
In any case keep domestic animals away, since to many (including dogs) this plant proved to be toxic on ingestion.

Thank you for your answer, but I don't think this is the one.


text:
Can you identify this species?

It is similar to a kinkajou but it isn't for sure. I would include it into carnivora, and then maybe canifornia but I really don't have a clue.

With Chrome, if you have a picture, you can do a right click on it and do a google image search. Doing so with the image you provided finds, amongst others, the wikipedia page for the Common spotted cuscus

The fruit seems to be Averrhoa carambola, oxalidaceae.

That's a marsupial, the spotted cuscus, Spilocuscus maculatus.
Here is another image:

By the way, the same individual in your photo can be found in this site about Australian animals, still eating that starfruit:


text:
Replication cohorts in microbial GWAS
Replication in an independent cohort is of course the gold standard in GWAS studies, and many high profile journals will now (quite rightly) not accept finding indicating a phenotype genotype association without evidence of replication.
However GWAS is no longer the domain only of human genetics and is being increasingly used on microbial species, pathogenic on humans, animals, and plants. However having read many of these studies (mostly in plant pathology) i can find no discussion of technical replication practices in their methods. In my own research I intend to conduct GWA between snps and gene presence-absence genotypes gathered by illumina sequencing, and phenotypes of virulence (as a continuous quantitative variable) when inoculated onto the host plant (which is wheat), of a large population of a fungal pathogen. i have inoculated 120 plants with 120 isolates of the pathogen, and i'm an additional replication cohort of 80 plants and isolates.
My question is, what is required to make these additional inoculations an 'independent' cohort?
The idea of independence in technical replicates is to correct for systematic bias present in the discovery cohort, I will likely grow these plants in a separate greenhouse bay for example (although since the different host-isolate combinations are randomised within the greenhouse even this may not be necessary); in a human GWAS different genotyping methods would be ideal in the replication cohort due to possible introduction of bias in the snp-chip, in my own study i'm unsure if this would be necessary as variants in my data will undergo stringent filtering prior to genotype calling.
If anyone could help point out to me what my possible sources of systematic biases are, i'd be very grateful.


text:
How much smaller is the diffusivity of a molecule in the retina as opposed to the vitreous of the eye?
I'm interested in the diffusivity of macromolecules inside the mammalian retina, relative to the vitreous.
For example is the diffusion coefficient for a macromolecule (protein, 50-150 kDa for example) 10 or 100 times smaller in the retina than the vitreous?
The diffusion coefficient for such a macromolecule is about 10^(-6) cm^2/sec in the vitreous - roughly that of a protein in water. I can't seem to find any information on how much smaller it would be in the retina, a tightly packed tissue.

Unfortunately, I don't have a good, simple answer for you. The reason is that the answer may depend significantly on details of the macromolecule more than its size - like how strongly it binds to the environment.
In addition, within an environment that is more elastic than viscous, and with a very complex shape, you might expect to get various sorts of anomalous diffusion, rather than a single diffusion coefficient.
Transport in tightly confined biological spaces is complex, and still pretty controversial. A paper I found useful as a simple introduction to some of this:
Morphogen Transport - http://dev.biologists.org/content/140/8/1621

Thank you! This is useful information. It's interesting that this is a controversial topic! I'm building a diffusion based model you see, so for my purposes I require some numerical estimate to compare between the two areas.
The macromolecules I'm interested are antibodies and fragment antibodies, which bind to VEGF, all these molecules are in the range of 50-150 kDa, and do not bind (at least for my purposes within the model) to any structures within the vitreous or retina.

It's an interesting issue! I recommend seeing what experimental data you can find for any sort of transport properties, but be prepared for there to be a significant spread (don't stop after getting the first estimate).


text:
What is the species name of this moth?
This insect was found in India. It looks like a hawk moth to me, but I still can't get the exact name for this species.

I believe that it is the vine hawk moth (Choerocampa rosetta).

https://www.whatsthatbug.com/2010/11/20/vine-hawk-moth/

Welcome to Biology.SE! It would be highly appreciated if you add some more details and some images for comparison. Link-only answers are generally not welcomed since links can get invalid if they break or the link address changes.

I would be happy to. Is there a way to copy/paste pictures into the answer or can I only do it through "upload"?

You can paste a link to the image. Just above the answer-editing box, there is an image button. When you click on it, you will get options to both upload an image as well as paste a link for it. If the site refuses the image format, you will need to upload it.