text:
Do humans produce rennin?
At school, we've been taught that human infants produce rennin/chymosin (which aids in the digestion of milk). More specifically, it is the peptic cells in the stomach which secrete prorennin, the inactive form of rennin (in addition to pepsinogen, the pepsin proenzyme).
User @another'homosapien's answer here also seems to concur with this (excellent answer by the way, I enjoyed reading it).
However
According to Mod. @AliceD's answer here (yet another excellent answer):

...in humans there is only a chymosin pseudogene present...

Which (probably?) implies that humans (infant or otherwise) do not produce rennin.
I managed to get my hands on the Textbook of Medical Physiology (Guyton and Hall, South-Asian edition), and according to the book (Chapter Gastric secretions, page 406) peptic cells produce a large quantity of pepsinogen. There is, however, no mention of prorennin. I even flipped over to the Appendix at the back to look up "Rennin", but it turns out there is absolutely no mention of rennin in the book.

My questions,

Some sources claim that rennin is produced in human (infants). Is this true?
Other sources claim that rennin is not produced in humans ( we have a pseudogene for it though). Is this correct (I mean the "rennin-is-not-produced" bit, not the "pseudogene" bit)?
If rennin is produced in humans only during infancy, what stops it from being produced as we mature? (I'm asking this because every source I've seen that claims that rennin is produced in humans, explicitly states that is done so during infancy...which would suggest that rennin is not produced in adults)

2 things: 1) Existence of a pseudogene doesn't necessarily mean a non-functional protein product, it just means that it differs from the gene being referred to. 2) Rennin exists to curdle milk and slow digestion (like in the answer you linked), it is not necessary for digestion of milk otherwise.

@Bryan Ah, thanks! Being the idiot school-boy I am, I assume "pseudogene" = "No proteins translated". ;P Also, I just want to know if rennin is produced at all. Thanks for the pointer anyway!

I clarified below and decided to turn my comment into an answer. It's quite possible someone will come up with a better answer but that was all I found so far.

Also, as sort of a tongue-in-cheek answer: actually humans (presumably primarily adults) produce tons of rennin, via recombinant expression in bacteria. It is quite important for producing most cheeses, and a lot more convenient than isolating from animal sources. :)

Scanning various reviews it seems that everyone who mentions the possibility of a human chymosin refers to a single paper. So for example this 2014 review has a single reference to a human chymosin:

Henschel et al. detected a
  protease in the gastric aspirates of newborn infants within 6–10 h postpartum that was not
  pepsin [62]. The electrophoretic mobility and immunoreactivity are similar to that of calf
  chymosin, a protease that cleaves κ-casein and causes casein curdling. This protease is
  unique in that it disappears from gastric fluid at 10 days postpartum and is not found in adult gastric fluid.

I don't have access to the Henschel et al. paper (from 1987) but here is the abstract:

The electrophoretic mobilities of proteases present in gastric juice taken within 10 h of birth from 5 healthy, premature infants were compared with calf chymosin, pig pepsin A and human adult gastric juice. The juice from 2 infants contained predominantly a chymosin-like enzyme, another had almost exclusively pepsins similar to those of the adult juice, while the other two contained a mixture of both. The pepsins consisted of two elements, probably pepsin A (EC 3.4.23.1), and pepsin C (EC 3.4.23.3). Single radial immunodiffusion gave a definite reaction to calf anti-chymosin serum in five samples taken from a further 17 infants. These results indicate that some human infants secrete chymosin. The reaction in the immunodiffusion assay indicated a much lower enzyme activity than that implied from electrophoretic separations. It is suggested that species differences resulted in poor cross-reactivity of the antiserum.

Now, obviously, without seeing the data it isn't possible to be conclusively critical, but the quality of the evidence seems to be rather weak, being based upon similar electrophoretic mobilities and an immunodiffusion assay (why not a Western blot?) with an overt apology for weak cross-reactivity of the antiserum used.
However, leaving all of that to one side, the strangest thing about this is the sporadic appearance of the proposed chymosin: although 4/5 were scored as chymosin positive in the 1st experiment, is it likely that 2 of these would apparently contain little pepsin? And in the second experiment (the immunoassay) only 5/17 scored positive for chymosin.
Evidently no-one has ever reproduced this result, and the evidence for the pseudogene (but no active gene) is very strong. I vote that humans do not produce a chymosin.
Update
Having read Bryan Krause's answer: if the human gene product was lacking an exon's worth of amino acid sequence then presumably it wouldn't have an electrophoretic mobility that was closely similar to the calf protein.

I think the answer is really that is isn't clear, though I only searched a bit and found mostly old papers.
It seems like people have found immunoreactivity to anti-rennin antibodies in human infants, but that doesn't necessarly mean rennin is present, just something similar (which could even be a totally unrelated protein).
On the genetics side, humans have a pseudogene for rennin (known as prochymosin), but if you take the same exons from that gene that are used to make rennin in cows, the protein would be truncated because one of those exons has a frame-shift mutation (this is why they are calling it a pseudogene). However, it is possible that there is a functional protein produced by that gene if that 'exon' is excised from the transcript (see the paper below).
Örd, T., Kolmer, M., Villems, R., & Saarma, M. (1990). Structure of the human genomic region homologous to the bovine prochymosin-encoding gene. Gene, 91(2), 241-246.

The psuedogene is not functional, according to Wikipedia: "Humans have a pseudogene for chymosin that does not generate a protein, found on chromosome 1." The reference for this says " Thus, this genomic sequence apparently represents a human prochymosin pseudogene. No functional gene was identified."

And yet some people claim that human infants do have rennin: if they do, it has to come from a gene, and this is the only candidate. It's pretty hard to prove definitively that it doesn't, which is why the statement is "apparently." I agree that it seems the most likely conclusion is that it does not produce a protein (note that the actual source for that statement in wikipedia on the pseudogene is the reference in my answer).

Ok.. I noticed the reference... I thought you were making the point that a protein was produced, although it is most likely not true...

Yeah, sorry, I was just trying to note that the answer by @AliceD about the presence only of the pseudogene does not by itself totally rule out the possibility of a human rennin. I think the other papers failing to find it is better evidence.

you mean @Alan Boyd...

@TanMath No I meant AliceD - the post the OP referred to. Oops - I had tracked down that quote to its actual post and meant to edit the OP to fix it. OP quoted from an answer but then linked to a different answer twice.

@Bryan Thanks for the answer! That the "answer isn't really clear" (though it's quite likely that we don't produce typical calf-rennin) became apparent after I read Alan's answer. Plus, the excerpt from the paper (Henschel et al.) in his answer made for an interesting read. Hence I've "accepted" Alan's answer. Your answer was very insightful, and I appreciate that you took the time to post an answer. Thanks a ton! ^_^

Way back in 1964 I was asked a question about Rennin in a physiology class. Perhaps you are not searching back far enough for information. Also, if the infant was not nursing on human milk there may not be a substance present to cause rennin production, if nursing on cows milk the substance that causes the production is not the same as in human milk so no rennin is produced. If all other mammals produce rennin it would seem that humans would also produce unless after several generations no stimulation has resulted in functional loss. One assumption you can always make is the body knows what it is doing. We discover scientific facts:God creates them.

Welcome to Bio.SE!  We're glad to see you here.  It would be much better if you could add some sources for your answer: as it stands it's a bit anecdotal and subject to removal.


text:
How do you derive steady-state conditions from the open-state differential equation of ion channels?
My books describes this differential equation for the open state of an ion channel:

Where $k$ are the rate constants,
$k_1$ denotes a forward reaction
$k_{-1}$ denotes a reverse reaction in the Markov model

$O$ is the open state, $C$ is the closed state.
According the principle of mass conservation
 $ C + O = 1 $
where $ C $ denotes the closed state
"From here, it can simply shown that under steady-state conditions that $O_{\inf} = \frac{k_1}{k_1 + k_{-1}}$
and the relaxation time constant of the reaction $\tau = \frac{1}{k_1 + k_{-1}} $ "
My question is, how are $O_{\inf}$ and $\tau$ derived?

Is this a homework question? If so it should be tagged as such and you should provide evidence of an attempt to answer it yourself.

@SheaBryan Did you mean to type $C$ instead of $V$ for the statement, "$C/V$ is the membrane potential, .."? I'm assuming you meant to type $C$, since $V$ is never used or mentioned otherwise. I am aware that voltages are involved, however, it seems to make more sense that you hit the adjacent key on the keyboard when typing this, since the usage of $C$ would be much more consistent to the surrounding statements of your post. Please correct me if I'm wrong. Thanks.

@Charles V wasn't important here, so I removed it; C is not the membrane potential its the closed state, such that C+O=1.

You changed V to C and called C "voltage". That's why I explained.

These are really math problems (algebra and basic calculus) rather than biology problems.
Oinf comes from solving algebraically the first equation you posted for steady state: i.e., when dO/dt = 0; just solve for O.
The time constant comes because this is a first-order exponential decay, which you get when you solve an equation (calculate an integral) of the form dO/dT = -lambda * O. The solution to that equation is an exponential decay of the form O(t) = O(0) * exp(-lambda*t)
tau is defined as 1/lambda and gives you the decay rate(relaxation time constant).

Always appreciate explanations for downvotes.

i guess answering bad homework question

@Charles I was trying to give OP some help without doing their homework for them. I understand the style preference, though.

My question is, how are $O_{inf}$ and $\tau $ derived?

".. it can simply be shown that under stead-state conditions .. " -- By specifically keeping in mind steady-state conditions, certain assumptions can be made when utilizing the mathematical model that the book proposes, which will ultimately allow for us to arrive at the conclusions regarding $O_{inf}$ and $\tau$.

To derive $O_{inf} = \frac{k_{1}}{k_{1} + k_{-1}}$
We'll utilize the differential equation that was provided by the book, and set $\frac{\mathrm{dO} }{\mathrm{d} t} = 0$, given the fact that we're considering steady-state conditions; i.e., a state of the ion channel in which its voltage charge and discharge have the same rate. By forcing the change in voltage charge & discharge to have a value of zero, we can solve for the steady-state voltage charge, represented by $O$.
$$\frac{\mathrm{dO} }{\mathrm{d} t} = 0 = k_{1}(1-O)-k_{-1}O$$
$$\:\:\:\:\:\:\:\:\:\:\:\:\:\:\:\:\: = k_{1} - k_{1}O + k_{-1}O$$
$$\:\:\:\:\:\:\:\:\:\:\:\:\:\:\:\:\: = k_{1} - O(k_{1} + k_{-1})$$

We'll now isolate $O$ by moving its terms to the L.H.S. of the equation, and then dividing by $(k_{1} - k_{-1})$.
$$0 = k_{1} - O(k_{1} + k_{-1}) $$
$$O(k_{1} + k_{-1}) = k_{1}  $$
$$O_{inf} = \frac{k_{1}}{k_{1} + k_{-1}} $$

Given that the book mentions conservation of mass when contextualizing the expression $C + O = 1$, it would seem that the result of this (mathematical) expression quantifies open (and close) state of an ion channel in terms of the number of ions that are not reinforcing the conductance state at a given time. I feel that this distinction is important to make because I've encountered this equation within other contexts, and each context brings with it different sets of assumptions that can and can't be made.

To derive $\tau = \frac{1}{k_{1} + k_{-1}}$
Again, we start with the differential equation, but this time we'll integrate. For ease of notation, we'll first make the substitutions $O = y$ and $\frac{\mathrm{dO}}{\mathrm{d} t} = y'$.
Beginning with an intermediate step from the previous section,
$$\frac{\mathrm{dO} }{\mathrm{d} t} = k_{1} - O(k_{1} + k_{-1})$$
$$y' = k_{1} - y(k_{1} + k_{-1})$$

and now applying separation of variables,
$$\frac{y'}{k_{1} - y(k_{1} + k_{-1})} = 1$$

We then use $u$-substitution to integrate the L.H.S. of the equation, where
$u = k_{1} - y(k_{1} + k_{-1})$ and $u' = -y'(k_{1} + k_{-1})$, which yields

$$ \int \frac{y'}{k_{1} - y(k_{1} + k_{-1})} = \int 1$$

$$-\frac{1}{k_{1} + k_{-1}} \: \int \frac{u'}{u} = \int 1$$

$$-\frac{ln|u|}{k_{1} + k_{-1}} = t$$

Solving for $u$, we have
$$- \: \frac{ln|u|}{k_{1} + k_{-1}} = t$$

$$ln|u| = \: - \: t(k_{1} + k_{-1})$$

$$u =  exp\begin{Bmatrix} - t \: (k_{1} + k_{-1}) \end{Bmatrix}$$
which is the same as
$$k_{1} - y(k_{1} + k_{-1}) =exp \begin{Bmatrix} - t \: (k_{1} + k_{-1}) \end{Bmatrix}$$

Now, solving for $y$ and back-substituting $O$ for $y$,

$$O = \frac{k_{1}}{k_{1} + k_{-1}} \: \: exp \begin{Bmatrix} - t \: (k_{1} + k_{-1}) \end{Bmatrix}$$

and noticing that $\frac{k_{1}}{k_{1} + k_{-1}} = O_{inf}$ we have
$$O = O_{inf} \: \: exp \begin{Bmatrix} - t \: (k_{1} + k_{-1}) \end{Bmatrix}$$

Lastly, we re-express the exponential argument as
$$- t \: (k_{1} + k_{-1}) = \frac{-t}{\frac{1}{k_{1} + k_{-1}}}$$

where $\tau = \frac{1}{k_{1} + k_{-1}},$ to then get
$$O = O_{inf} \: \: e^{-t/\tau}$$

which fits the form of the exponential decay equation, $N(t) = N_{0} \: e^{-t/\tau}$, where $N = O$ and $N_{0} = O_{inf}$, and $\tau$ is defined to be the average length of time that an ion remains unchanged by the conductance state of an ion channel at a given time $t$.

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Why do germs live longer on surfaces than on skin?
After looking up how long germs live for on surface, I came across lots of resources that explain how long germs live on different surfaces.
A common pattern is that germs survive longer on cold/hard surfaces than on skin.
Why is that?
Wouldn't skin be a much more hospitable environment than something like a desk?

I'm pretty sure that will vary a lot from a surface to another. Can you please develop stating what surface you are talking about and also linked to your sources.

Not only will it vary from surface to surface, but will vary with microorganisms as well. I think this is too broad. If you can narrow it down to one microorganism, or provide your source, this might be better.

because some skin cells which are alive , secret fat and other materials , these materials make the skin acidic , and acidic environment is not good for many germs , on the other hand , there is an enzyme in  sweat (lysozyme)which destroy the wall of bacteria

Source, please?

My explanation is partly mentioned in ,junqueira basic histology , chapter skin , part protection and sweat glands , but the whole explanation exists in a book which was taugt in my college and that is not a reference book, unfortunately.

You might be an ESL (so am I) but please note that in english (and in most other language using the lating alphabeth), sentences start with a capitalize letter and end with a dot. Comas are not preceded by a space and closing parenthesis are followed by a space. Don't forget to conjugate your verbs (destroy). I think you meant secrete and not secret.  we dont write like dis on StackExchange. The term germ is never use in Biology. I suppose you meant pathogens.

Ok, thanks for your attention. I will be more careful next time.

@Remi.b I'm only linking this because of your use of the word "never", and the fact that it has 1500 citations. I do agree though, that I don't like the word "germ".

@Bob You're right. I should have said rarely. Germ is quite informal.

@minasi Btw, if english is not your mother tongue, I'd be curious what language actually puts spaces before commas.

@Remi.b, as far as I remember there was a rule for this site which told us we can not use abbreviations in our texts just like btw.

@Remi.b, no language puts space bofore commas. I told you it was all my mistake and this is because I focused on concept of my sentence.

Some of the permanent microbial flora inhabiting the skin protects the host from other pathogens. The complex host– microbe and microbe–microbe interactions that exist on the surface of human skin illustrate that the microbiota have a beneficial role, much like that of the gut microflora. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746716/
It is apparent that just as host immunological factors and behaviors shape the composition of these communities, microbes present on the skin greatly impact the functions of human immunity. Thus, today the skin immune system should be considered a collective mixture of elements from the host and microbes acting in a mutualistic relationship. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219649/
Eccrine sweat glands secrete water to the surface of the skin. The water also contains salt and electrolytes which work to acidify the skin. This makes the skin a cool, dry, and slightly acidic barrier.
Furthermore, eccrine sweat glands constitutively express several antimicrobial peptides (AMPs), including cathelicidin and β-defensins. - https://www.ncbi.nlm.nih.gov/pubmed/16374474
Together, these factors are the reason why a desk would be more hospitable for some microbes

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Are insects capable of gliding on the air with their wings spread, similar to birds?
Sometimes birds can use the air to float on with their spread wings. Now, the wings of insects are too small to see if they can do that too. So is it possible for insects to do this also, or can't they hold their wings spread or is the air drag not enough?

"Insect" is a very broad catagory.  Simplistically, some can: ever watch large butterflies?  Just as some birds, like hummingbirds, can't glide well, if at all.

It's worth mentioning that insects' flight is somehow different from birds' one, mainly because of the Reynolds number.
However, there is evidence of (some) insects gliding. For instance, Walkeling and Ellington (1997) have filmed gliding in dragonflies and damselflies:

The free gliding flight of the dragonfly Sympetrum sanguineum was filmed in a large flight enclosure. Reconstruction of the glide paths showed the flights to involve accelerations. Where the acceleration could be considered constant, the lift and drag forces acting on the dragonfly were calculated. The maximum lift coefficient (CL) recorded from these glides was 0.93; however, this is not necessarily the maximum possible from the wings. Lift and drag forces were additionally measured from isolated wings and bodies of S. sanguineum and the damselfly Calopteryx splendens in a steady air flow at Reynolds numbers of 700-2400 for the wings and 2500-15 000 for the bodies. The maximum lift coefficients (CL,max) were 1.07 for S. sanguineum and 1.15 for C. splendens, which are greater than those recorded for all other insects except the locust. The drag coefficient at zero angle of attack ranged between 0.07 and 0.14, being little more than the Blassius value predicted for flat plates. Dragonfly wings thus show exceptional steady-state aerodynamic properties in comparison with the wings of other insects. A resolved-flow model was tested on the body drag data. The parasite drag is significantly affected by viscous forces normal to the longitudinal body axis. The linear dependence of drag on velocity must thus be included in models to predict the parasite drag on dragonflies at non-zero body angles. (emphasis mine)

Source:

JM Wakeling, CP Ellington, Dragonfly flight. I. Gliding flight and steady-state aerodynamic forces. Journal of Experimental Biology 1997 200: 543-556.

Good find this article! I spend quite some time in the field observing dragonflies, and from this experience I can verify that at least some dragonflies alternate active flight with short gliding (few seconds). I observed this only in large aeshnidae, like Aeshna viridis and Anax imperator. I can't remember seeing it in Calopterix or Sympetrum, although these are very common here. But if these smaller species glide for very short times, this may be difficult to see without camera footage.


text:
Why doesn't ovulation occur in both ovaries simultaneously?
I know that in human body ovulation takes place at only 1 ovary every month. But development of a follicle depends on FSH levels in the blood, and since both the ovaries are exposed to the same blood supply, how does it make sense for development of follicle to be seen only in one ovary? Aren't both ovaries exposed to same FSH levels every month?
I am not able to figure out the solution to this anomaly and would appreciate some answers.

I don't know the answer to this but it could simply be that once an ovary has ovulated it enters some sort of refractory period so that it ends up skipping a cycle.

@AlanBoyd - Ovulation isn't democratic. Each ovary has an equal chance of ovulating every cycle. I don't know why that is, but it is.

@anongoodnurse I had got the idea that they alternated.

Each ovary has hundreds of thousands of follicles. And, of course, each one of those follicles is exposed to the same blood supply.
Therefore, your question...

Why isn't ovulation seen in both ovaries together?

... is the same of:

Why isn't ovulation seen in two follicles (regardless the ovary)?

All follicles are stimulated by FSH and they indeed start to mature at the same time. However, in a given cycle, normally only one follicle fully grows1. What we have here is a competition among follicles.
Guyton is not my favourite book on physiology, but it suggests an explanation for this:

Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia:
After a week or more of growth — but before ovulation occurs — one of the follicles begins to outgrow all the others; the remaining [...] developing follicles involute (a process called atresia), and these follicles are said to become atretic. The cause of the atresia is unknown, but it has been postulated to be the following: The large amounts of estrogen from the most rapidly growing follicle act on the hypothalamus to depress further enhancement of FSH secretion by the anterior pituitary gland, in this way blocking further growth of the less well developed follicles. Therefore, the largest follicle continues to grow because of its intrinsic positive feedback effects, while all the other follicles stop growing and actually involute.
This process of atresia is important, because it normally allows only one of the follicles to grow large enough each month to ovulate; this usually prevents more than one child from developing with each pregnancy. The single follicle reaches a diameter of 1 to 1.5 centimeters at the time of ovulation and is called the mature follicle.

Therefore, the reason why we don't see both ovaries ovulating at the same time is the same reason why we don't see one ovary ovulating twice at the same time: the fastest growing follicle inhibits the growth of the other follicles (in the same ovary or in the contralateral ovary, it doesn't matter).
Besides that, it also explains the pattern of ovulation: in a given cycle, the left and the right ovary have equal chances to ovulate. Thus, the ovaries don't take turns like this (L is left and R is right):
L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R → L → R etc...
The real pattern is probably random:
L → L → R → R → L → R → R → R → L → R → L → R → L → L → R → L → L → L ETC...
According to Ecochard (2000):

It is concluded that in normally fertile women, the cycle length and the hormonal profile are independent of the, most probably random, site of ovulation. (emphasis mine)

Sources:

Hall, J. and Guyton, A. (2011). Textbook of medical physiology. Philadelphia, Pa.: Saunders.
Ecochard, R. (2000). Side of ovulation and cycle characteristics in normally fertile women. Human Reproduction, 15(4), pp.752-755.

1Note that, for answering this question, we will (wrongly) assume that there is no polyovulation in humans. However, as polyovulation does occur in humans, ovulation can sometimes be seen in both ovaries.

Unrelated: "Guyton is not my favourite book on physiology...". Why so? Also, what book would you recommend instead? (I use Guyton to clear physiology questions that I have...if you know if a better book, I'd love to hear it from you!) O:)

My favourite is Ganong (the old editions). It doesn't mean that I recommend it, it's just a matter of personal choice: I like Ganong better.

I see! Is there any particular reason for your preference? Is it...well...more lucid? or very detailed? or something? (I'm still a high-schooler, but I'm inclined to choosing the medical field. Someone recommended I keep a copy of Guyton handy. It's a good book, but I won't mind being recommended a few more) Sorry for bugging you again! ^_^

Ganong gives more detailed explanations at the biochemical level. However, it's harder to read if you don't understand physiology. On the other hand Guyton is easier to read, and covers way more ground.

So u guys  are basically saying the whole left right theory is incorrect and that it is a random process

@AdithyaEshwarla Yes, it is a random process. Also, since the "left-right alternating" is incorrect, it's not a "theory".


text:
How is DNA testing used to differentiate between different species?
How is DNA testing used to determine that specimens belong to different species, rather than being subspecies, or members of the same species?
Usually the definition of species is about the ability to produce fertile offspring under natural conditions. How are markers chosen that indicate individuals are different species?
Or does this process occur the other way around? Are species identified as being different, then DNA used to identify which members are which?

Statistics of divergence
You can compute various statistics of group divergence. Typically you could consider the pairwise number of differences between any pair of individuals. For example the following two sequences
ATATATCCTGTGTCA
AAATATCTTGTGTCA
has 2 differences.
Obvious or obscure grouping
Often, individuals really group together quite naturally (if you perform a principle component analysis you will see clearly defined groups) but sometimes the groups are quite blurry.
The definition of species is arbitrary
Whether the grouping is blurry or not, it is often quite arbitrary how much two groups need to be different in order to classify them in different populations, different subspecies or different species, different genera, etc...
The problem here is more a problem of definition than a technical problem. You should have a look at this post to understand the issue behind the definition of species.

My attempt at a high school level explanation
Explain what a phylogenetic tree is
First draw a phylogenetic tree. Explain what they mean:

A node is an common ancestor
A leaf is a extant species (if the leaf gets to the top of the tree)
All species are related but some are more related than others..
Introduce the concept of sister clade
Explain that every species in a sister clade is equally related to the all the species in the other sister clade by highlighting their common ancestor.
Explain that no extant species is the ancestor of another species as the ancestors are the nodes.

You can get a short introduction to phylogenetic trees here on Biology.SE or here on Understanding Evolution.
Methods to reconstruct a phylogenetic tree
Let them wonder how we could get to know what the true phylogenetic tree is.
Suggest using phenotypic data and make them realize and if you put all the yellow flowers together, or the flying organisms (insects, birds, bats, squirrels) it won't work very well. So phenotypic data can sometimes be misleading. So explain that we can use genetic data by counting the number of pairwise differences. Let's consider the three different sequences
species A: ATCTCTG
species B: ATCTCTT
species C: AGGCATT
It sounds like the first two sequences are more closely related than any of them are to the third sequence. You can draw the tree for these three species.
Molecular clock (optional)
Knowing the rate at which mutations occur, one can date since when two lineages diverged based on genetic data. You will probably have to learn a bit more about molecular clock for yourself. You may ask a for high school explanation in another post.
Within population diversity (optional)
Recognizing the existence of genetic diversity within population is key to all evolutionary processes so it is good to let them understand the existence of such diversity early on.
Of course there is genetic diversity within a species that renders everything a little bit more complicated. For example, some of you have blue eyes while others have brown eyes (assuming there is variation for eye color among your students), this is due to the fact that the DNA sequence within each of you is a little different. Not as different as it is between humans and chimpanzee but a little bit different.
Genetic data to group populations into species
Then, you can say that genetic data can allow us to tell groups apart. You can show a PCA type of plot (without really explaining what a PCA really is) with colors. Each color correspond to a population (insiste on term population and not species). Something like

and then argue informally that light-yellow, green and red populations are probably different species while all the other populations seem to belong to the same species.
Problem with the species definition
If you really want to bring the question of the how to use genetic data to tell species apart, then you will first have to destroy their concept of species! For that, you should first have a look at this post. You will have to

Introduce the biological concept of species
Explain why this concept does not work for asexual species (hopefully they know that many species are asexual).
Give an example of another issue such as the classical (yet rarely observed) example of ring species (see here on Biology.SE or here on wikipedia)

Then, get back to the PCA and ask, how different two populations must be for them to be called different species? And make them realize that this is rather arbitrary. We can tell they are different lineages but it is up to everyone to decide what we want to call a species. However, very often vague intuition about how different a species should be is good enough.

So the description in the media, and in high school science of the use of DNA testing to identify new species from closely related groups is a gross over-simplification? I'm asking as a science teacher grappling with this content having recently been added to the curriculum.
If a student were to ask for clarification, I'd be trying to explain how DNA testing showed the samples were different enough to be considered different species, but have no way of (in appropriate level language) explaining what 'different enough' is and how it is determined. Can you simplify for high school audience?

@Jakra Answer edited. Let me know if my edit helps! It is good to see a high school teacher that bother to teach well and right.

That's really helpful! PCA is fine, its part of the curriculum anyway, it was the statistical analysis that I wouldn't have been able to explain. Your graph and explanation are going to be very helpful.


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Using Transduction to reverse Antibiotic Resistance?
Is it possible to use reverse transduction to reverse antibiotic resistance. Since antibitiotic resistance is causee by transduction of the F factor, is it possible to induce a F+ non antibiotic resistant bacteria into a region of F- resistant bacteria?

This seems very confused. Apart from anything else, The F plasmid doesn't encode an antibiotic resistance. Are you asking if it is possible to get rid of a plasmid from a bacterial strain?

@AlanBoyd Wait is it the R plasmid? Hmm I guess so... My question is whter we can make resistant bacteria transfer genes with non resistant bacteria.

https://biology.stackexchange.com/a/64618/6307

OK bacteria with an F plasmid can transfer their other plasmids (which may encode antibiotic resistance) during F-mediated conjugation. Now, starting from there, what is the question?

@AlanBoyd i think canadianer's link has already answered my question . Thanks anyway!


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Identify insect found in cupboard
Opening the cupboard I am shocked to find it full of these insects inside. Haven't found them anywhere else. At first, I thought it was ticks, but not so sure. Plan on cleaning out the cupboard and using Bifen I/T to hopefully kill them.
I live in the Caribbean and would like to identify and find out how to get rid of them.

You should add tag species-identification. It can help other people to help you.

Looks like some sort of weevil to me.

This is just a rice weevil, Sitophilus oryzae: https://en.wikipedia.org/wiki/Rice_weevil, or maybe a maize weevil, Sitophilus zeamais.

@GerardoFurtado I agree. Is there any reason you're posting that as a comment rather than an answer?

Yes, two reasons: first, I was just about to turn off the computer. Second, the user above my comment identified it first, so he deserves the answer.

I wouldn't have been offended if I had commented "weevil" and you had made your more detailed response an answer. I see a big difference between a quick first impression and a reference to a specific species. :)


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

You might explain what Pillayar and Vinayagar are, for the benefit of those who aren't that familiar with Hindu culture.  But closely-related species can produce offspring: mules, wolf-dog,coyote-dog, and coyote-wolf hybrids, ligers and tigons, "beefalo" (cow-buffalo), and more.

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


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Why do humans grow taller than their ancestors?
I'm taking the Introduction to Genetics And Evolution course and in the first lecture it was said that:

Evolution in a biological sense is simply a change through time. And very importantly, that is change through time over generations. So for example, the human species, hundreds or thousands of years ago was much shorter than it is today. Over the course of those generations, the human species has grown taller. That change is an evolutionary change.

I'm wondering why we become taller than our ancestors? Now we almost don't fight with other species and can live doing something that doesn't require physical strength. It's more logical to me if we would become shorter.

Humans compete with each other. The competitor doesn't need to be a different species - it can be a different population, different individuals in the same population, or even just environmental conditions (e.g. moving to colder or warmer climate). Indeed, competition within the species has a huge benefit - it can cause runaway improvement since you're always competing with the best of the given generation. This is one of the explanations for why human intelligence seems to be so far ahead of anything our "species-relatives" have, by the way.

@Luaan conspecific competition can have the effect of reducing competitive abilities with other species. Also, technically, there is no need for competition for selection to happen (even if completely isolated, some genotypes may still be associated to higher fitness than others).

The human species has grown taller since the last 150 years, especially after 1950. During the world wars the humans (at least in Europe) declined in height. In some poor African countries the people are now shorter than they were 40 years ago. It is a lot about nature and nurture.

Yes, worth noting that some of the increase in height (especially recently) is phenotypic (environment) rather than genotypic (evolutionary) (I would hope the course material points this out!)

Related: https://biology.stackexchange.com/questions/457/height-and-natural-selection-in-humans/ and https://biology.stackexchange.com/questions/19101/are-asian-people-genetically-predisposed-to-be-shorter-than-europeans

A likely misunderstanding of yours

Now we almost don't fight with other species

Misunderstanding about selection
As you will go through this course, you will understand why this sentence makes little sense. A change in allele frequency via natural selection is caused by a fitness differential among genotypes within a population. The existence of a competitor species would eventually affect this fitness differential but there is no need for a competitor for having a selection pressure.
I think you are having the view that selection is a process that allows a species to be better at coping with a competitor but this is wrong. Selection will increase the frequency of individuals having high fitness in the population. The resulting population may well not be a better competitor.
False opinion that we are not competing with other species
Also, about nearly 50,000 people are dying every day from infectious disease (UN press release). So, we are definitely still "fighting" with other species. Adaptation to malaria in humans is a famous case study (see this answer and its links).
Also, according to reuters (who fail to link to their source), the worldwide cost of pests in agriculture is estimated to about 540 billions USD per year! So yep... competition there is.
What selection pressures are there on human height?
Review paper recommendation
Stulp and Barrett 2016 is a review paper on the evolution of height in humans that you might want to have a look to have a clearer picture than what I will give here. It is easy to read. I highly recommend having a look at it.
They cite a lot of papers. I won't cite them again below but I will just attempt to make a vague summary of the parts which I think will interest you the most.
What selection pressures are there on human height?
The question appears to not be that easy to answer. In humans, height is highly heritable and there is a lot of variance in height among populations. It is likely that different selection pressures may have acted on different populations.
There are a diversity of selection patterns
In short, selection pressures on height include intra and intersexual selection. Taller adults seem to have a reduced mortality rate. Taller women have a lower risk of complications when giving birth. However, in both men and women, the correlation between height and number of offspring varies a lot from study to study (and likely from population to population). In the USA for example, men having the highest number of offspring are of intermediate height (balancing selection).
It appears that epigenetic variation also have an important impact on height Simeone and Alberti 2014 and there might have a sex-driven intra-locus conflict on height (Gilks et al. 2014; Stulp and Barrett 2016)
There is evidence of current selection on height
We have a fair number of evidence that height was and is still under selection in humans but we think that the exact pattern of selection pressures acting on it is quite complex. Note that there is evidence that height is still under selection today.

Stulp and Barrett 2016 link has limited access.

It's a pleasure to read your answer. I tried to give an answer, but as a non-native English speaker couldn't summarise it so nice. Especially I like the terms you use, lke selection pressure.

@cezar Thank you. Selection pressure is a very standard term in evolutionary biology.

@Artmal My link was broken. Sorry about that. Can you try again? There might have pay wall though.

@Remi.b I don't doubt that. I, as non-native English speaker, couldn't translate back to it. It's hard to discuss using technical terms you have learned in another language.

In my opinion there is a fallacy in your understanding of evolution. First of all evolution is blind to the future. Also living organisms don't undergo evolutionary changes toward something that might appear more logical.
Imagine there were only few tousands exemplars of Homo species left and the planet Earth would change so much that 90% of its surface is under water. It would be practical to have webbed hands. An exemplar with webbed hands could swimm better, and consequently be better equipped to provide food.
So what's going to happen. Are the humans going to develop webbed hands? Certainly not. It's not how evolution works. Just because something appears to be logical or of use, it's not going to come overnight.
But now imagine because of a certain mutation some exemplars have webbed hands. They are more likely to survive in an environment with large water surfaces. Therefore they are more likely to leave offspring. Exemplars without this mutation wouldn't be able to gather so much food, to escape from predators, etc. Eventually after millions of years they might all die out and only exemplars with webbed hands are existent. Then all humans would have webbed hands. The genes responsible for normal hands as we have, are almost not existent in the population.
After further millions years the water masses have retreated and there is much more land surface. The evolution was blind for this. The humans continue to have webbed hands, although they aren't so practical anymore. Eventually a mutation occurs again, or some exemplars with recessive genes for normal hands have offspring. This offspring now has better chances to survive and in the course of many generations there is a substantial part of the population with normal hands.
The humans are today much taller than earlier, because it must have been of evolutionary advantage for very long time. In order to get shorter as a species, the environment (and also other factors) should favour this.
We have food in abundance, good medical care, and most of the offspring can survive to adult age. This enables most of the people can unfold their full genetic potential and grow taller. The humans (at least in the western world) consume milk after the weaning. It contains growth hormons and stimulates the growth.
In order to get shorter in average as species, the shorter exemplars should be able to live longer and leave considerably more offspring, and there should be evolutionary drawbacks for taller exemplars to leave enough offspring.
Do we have those conditions? No. That is why we don't get shorter.

We have food in abundance, good medical care is this also an opinion of yours? Half of world wide infant death is caused by malnutrition (Walker 2008)

No, it's a fact. In the western world (Western Europe, North America, Australia and New Zealand) there is food in abundance and good medical care. The tallest people live also in these regions, the Dutchmen leading the ranking. The shortest people live in poor countries. There are certainly some outliers, like the Maasai in Tansania. Food isn't only factor favouring the growth, but it is an important one. There are differences in the height within same populations like rural vs. urban India, North Korea vs. South Korea. I'd say they are result of better living conditions.

I did not notice (at least in the western world) at the end of your sentence, sorry. You can't draw a general conclusion based on a cherry picked population though. The review I link clearly indicate that there is selection favouring small people in some populations.

I have yet to read the links you provided, but I don't doubt that there are circumstances that would favour smaller exemplars in certain populations. My point was that availaibility of food during the childhood and the adolescence stimulates the growth. Why should people become smaller when they have the possibilities to unfold their genetic potential. The people in the western world became significantly taller only after the II World War. Until the 18th century the people weren't (much) taller than our ancestors in the stone age.

I'd also like to add that there is a ceiling and once the genetic potential has  been fullfiled, the average size isn't going to increase indefinitely. It's very unlikely that further improvement of the living conditions can lead to humans with height of 2.5 meters (it might be however rather 250 kg).

There is a negative correlation between female height and reproductive success in the USA. Nutritional stress lead to a negative correlation between height and survival as well. These patterns really vary a lot and it is not so easy to summarize them in a few simple sentences.

Sure, strong directional selection may yield heritability to reach 0 but variance is still very high in humans. If this sentence is unclear to you, you'll want to read this post

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


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Oregon - Tree Identification
Western cascade forest, definitely was planted. In a clearing in the forest along with some western red cedars. I couldn't find anything that would match it when looking for native Oregon trees.

Nice pictures! +1

I'm thinking this is a Taxus brevifolia, otherwise known as a "Western Yew". They're most commonly found in the northwest region of the United States; so, even if the tree was planted, it's quite probable that it was still acquired (somewhat) locally.

I had a difficult time finding an image that so directly matches the bark image you provide, just from where that tree is so young, but I was able to find a matured version of the tree, which still has a similiar color and bark pattern. I believe that when the tree matures, the vien-like bark sheds, which results in the "scarring" that can be seen in the following image.

And then here's a few images that show the foliage. Notice the similarities in how the pines flare out, and the coloration of the branches. Once your tree matures, it'll get darker in color and develop small red berries, as can be seen in the following images.
The mature tree is on the left, and the right is still developing (which is most accurate to your images).

There is a small chance that the species provided by this answer is inaccurate, but I'm sure it's at least within the Taxaceae family.

I think Charles is probably correct, but if it is planted then another possibility could be a Tsuga, although the green young branches lean me towards a Taxus as well. Also the presence of dead leaves that persist points to Taxus, where as a dead Tsuga will tend to shed its leaves quite quickly, whereas a Yew does not.


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Why does cell waste energy in meiosis, between meiosis 1&2
As far as I have learnt about meiosis I have read that anaphase 1 is followed by telophase 2 where chromosomes change back to reticulum.but in the very next stage i.e prophase 2 they again start condensing to form chromosomes again.i have also heard that is most species, cytokinesis is simultaneous and not successive( which means that the 4 cells undergo cytokinesis together)..
If this is the case, then what is the need for a cell to waste its energy on making chromosomes back to reticulum at the end of meiosis 1, and again condense it in the very next step
Can't it directly continue on to prophase 2!
It sounds ridiculous,...but I beleive there must be a reason behind it, because the last thing a cell would want to do is to waste its energy in such things.
Thanks in advance

Can someone please give an answer

There is a phase between meiosis 1 and meiosis 2 called Interkinesis.
During this phase centrosomes or centriole pairs undergo replication in animal cells, which is important for bringing true haploidy.
Refer - meiosis-ii


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Book for artists' renderings of extinct species?
I'm looking for a collection, in print or online, of pictures of ancient extinct species (i.e., imagined from fossil remains). Is there a good single resource for this? I'm interested in animals of all kinds, barring dinosaurs, and invertebrates. I'm not interested in recently extinct species but rather the very distant past.

Any clade you are particularly interested in? Are you interested in plants? In animals? In Vertebrates? In mammals? Are you interested in a particular mass extinction event? Past 100,000 years or older like dinosaurs (230-65 millions years) or even older? You don't necessarily have to narrow down your question but you might be disappointed to get drawings of ferns, of gigantic dragonflies or of dinosaurs if you were expecting mamooths, saber toothed cats and dodo birds.

You're absolutely right, I should have been more specific. I'm interested in animals of all kinds, barring dinosaurs, and invertebrates. I'm not interested in recently extinct species but rather the very distant past.

With a quick search I was surprise that I could only find

Animals of a Bygone Era: An Illustrated Compendium
Extinct Species
Extinct Animals of the British Isles
Extinct Birds

It looks like there is an open niche to someone who like biology of extinct species and illustrations!
Note all will be of interest to you. None of them seem to offer good quality computer based illustration but rather pencil drawings.


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How large are the inner ear hairs?
I was always under the impression that the auditory hairs located deep within the ear, past the ear drum, are microscopic.
After taking a shower today, I was softly padding my outer ear with some tissue paper to dry any moisture, when some wax just got attached to it. What was unusual was that there were some hairs on it (3-5 perhaps, overlapping) that were about half a centimeter in length.
Are these just regular hairs that grow in the inner/outer ear? Or are they the ones that actually aid in hearing (the ones I thought were microscopic).
My question is to verify whether or not these hair shafts I observed are used in auditory perception. Either way, are these supposed to fall off?

Those are just ordinary hairs growing in your ear, like the kind you find in your nose and, if you are fortunate, on the top of your head. The "hair cells" of the inner ear aren't really "hairs" at all, they are totally different, and you would never find them falling out of your ear.
Hairs like on your head are protein filaments produced by follicles in the skin.
Hair cells in the inner ear, on the other hand, are sensory epithelial cells with stereocilia, which are protrusions of the cell membrane. Those membrane protrusions have mechanically gated channels which are coupled to nearby protrusions; when the whole cell is pushed one way or the other, that influences the mechanical stress on those channels and they open and close, which produces an electrical signal that can be sensed by the auditory nerve.
These special 'hair cells' are way way deep in your ear, past your ear drum, past three little bones that conduct sound into your cochlea. If you are touching those, you are in bad shape indeed - this is very very unlikely under normal circumstances.


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Is it possible to label a DNA molecule using a radioactive sulphur?
The radioactive labelling of the DNA molecule is possible using radioactive phosphorus and tritium atom. But is it any how possible to label the DNA  molecule using a radioactive sulphur atom?

@AliceD I honestly don't understand the argument that his question isn't about biology. I can't really think of any reason to label DNA this way that wouldn't be part of a biological experiment. (of course adding the motivation would improve the question, but it is not necessary to make it on-topic in this case).

@MadScientist point taken. I'll remove the comment. However, adding background helps to add the 'prior research component' too. It would just greatly enhance question quality.

Yes, it is possible, and indeed this was the standard labelling procedure used in early Sanger sequencing.
You synthesise DNA using a deoxynucleotide with a sulphur replacing an oxygen on the α phosphate as shown below. This phosphate forms the phosphodiester link in nucleic acids so the sulphur is incorporated.
The image is of dATPαS

response to David's comments
Please note that:

DNA does not normally contain sulphur.
This technique is for in vitro labelling of DNA; as far as I am aware it isn't possible to label with sulphur in vivo.

I have down-voted your answer as the radio-active molecule produced by the method you suggest is not chemically DNA but an analogue thereof.

Please go to chat for extended discussions. Because of raised flags and the general negative tone,  I've removed most of the comments here. Please keep it civil.

http://www.nature.com/nchembio/journal/v3/n11/full/nchembio.2007.39.html


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What is this anise smelling plant?
On holiday in southern France and we found this small plant growing out of some rocky soil:

It smells quite strongly like anise but seems to be a different plant?

There are several plants in the family Apiaceae with these kind of thin leaves, and some smell strong and/or are used as herbs in the kitchen. This must be Fennel  Foeniculum vulgare, because you describe it's smell as anise. Dill looks similar, but smells different. Fennel is indigenous to the mediterranean, but planted all over Europe.
It can be quite big, but on poor, rocky soil might remain small.
Picture of fennel from Dutch wikipedia:

Looking at more pictures it does seem very similar, this would be an absolutely tiny fennel plant though


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Interpreting qPCR curves: how to find Ct value in my case?
I am reading my qPCR results and having no idea why Ct value is returned like this:

This is the qPCR curve of my samples, and the software returned Ct values of most of the curves as seen: 33.99-38.4 for the curves that have lower baseline.
The problem is the 2 curves (navy and black) with higher baseline at the first place. I read Ct values of these curves as 32-33, but the software says that the Ct values are 35.4 for these curves.
What could be the problem and what would be the right answer, my values or the software's?
Thanks in advance!

The software is correct. $C_t$ values are chosen to be sufficiently above background. As you can see, the background level is very different for two of the curves, so you can't use the same signal threshold for determining their $C_t$.

Thanks! I understood that the threshold for the black and navy curves should move up as the baseline is higher.


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What are these Insects?
I live in my hostel in NIT Tiruchchirapalli, in India. My hostel is infested with these beetle-like insects.

These insects posses a hard shell, if you flick them off the wall, they make a "tap" sound when they hit the ground. They're capable of flying but mostly stay on walls, sometimes even motionless. They also seem to be rather stupid, even for an insect. They don't attempt to escape even in life-or-death situations
tl;dr
What are these insects?

they are definitely beetles. size is important to know, and a better picture would be helpful too.

@picapica They're approximately 0.8cm from head to abdomen. I can't get a better picture as my phone camera can't focus that close up.

I'm trying to answer my own question. I did a bit of searching, and I found out that my insect resembles the Mupli beetle the most. From Wikipedia:

The Mupli beetle, Luprops tristis (ഓട്ടുറുമ in Malayalam), is a plant detritus eating Darkling beetle found in parts of India. The adult beetle is black and around 8 millimeters (0.31 in) long.

I hope someone can verify if my findings are correct or not.

Tenebrionidae is correct. Your ID may be correct.


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What is the name of this fruit?
I have attached a photo. I know the Nepali name for this fruit but not its common name in English and its scientific names. In Nepal we call it as 'lahare Aanp' (meaning Climber Mango). This fruit is a climber type like cucumber.
Does anybody know its common name in English and its scientific name?

Note that you can easily find the answer by using Google's image search feature. It returns a partially completed version of this drawing, https://scontent-lga3-1.cdninstagram.com/t51.2885-15/s640x640/sh0.08/e35/20837253_1095238210612152_3434464044126306304_n.jpg , which is labeled "Coloured Pencil Passionfruit wip".

This is a passionfruit. It comes from a plant whose scientific name is Passiflora edulis.

It's indeed a climber, as you can see:

Finally, a curiosity about the name passion fruit. The fruit is called passion fruit because the flower is called passion flower. This is the flower:

But why it is called passion flower? Passion here has nothing to do with sexual love or desire, the common meaning of "passion", but with the suffering of Jesus.
Some say that it's because the flower resembles (?) the crown of thorns placed in Jesus' head. Other say that it symbolises Jesus' wounds. In fact, in portuguese we call it "flor das cinco chagas", or flower of the five wounds.
EDIT: thanks to @AlanBoyd's comment, you can see that its connections with Christianity are way more complex: https://en.wikipedia.org/wiki/Passiflora#Etymology_and_names

Post Scriptum (not related to the question): this plant is native to Brazil, and I had a couple of specimens in my yard. One of the most interesting things about passionfruits in Brazil is that it attracts an insect that we call "percevejo do maracujá", or passionfruit bug in a very free translation. Its scientific name is Diactor bilineatus, and it's one of the most beautiful insects to me. I loved to see them feeding on my passionfruits. This is the adult on a passionfruit (where you normally find them), and the nymph is even more colourful:

+1 and confirmed here (if links to Google books actually persist).

@AlanBoyd good investigative skills! I actually identified the fruit straight away because I'm from South America, where Passiflora is native.

The Christian connections with the name are much more elaborate.

Indeed! I added that link to the answer, thanks.

Do you know any (free) database for species names in various languages?

In South Africa it's more commonly referred to as Grenadilla

@pufferfish: Thank you! "Granadilla" is the word I've been looking for for a few years now. I forgot what we called it back in ZA.

The flaps on the hind legs of the insect are quite intriguing.


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Why does the ova remain viable for only a day after ovulation?
The ova remains viable for approximately 24 hrs after ovulation to be fertilised by a sperm.

...chances of becoming pregnant increase dramatically if you have sex during the 5 days before ovulation and the 24 hours after ovulation.
  [source]

My question: what prevents it from remaining viable for a longer period?
My assumptions:

Could be because it is arrested in metaphase II so cannot undergo transcription
Could also be because its haploid
Due to progesterone effect.

So what is the real phenomenon behind this? Also note that, compared to the ova, the sperms remain viable in the female reproductive tracts for a longer time (approx. 4-5 days).


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What is the medical definition of death?
What is the medical definition of death? And how do medical examiners determine whether a person has really deceased, as opposed to for example a condition like brain death?

I think is mainly opinion based. Even medically there are different definitions  or versions of death (cardiopulmonary death and brain death).

Your question has been asked in a similar form before. Check out this thread: https://biology.stackexchange.com/questions/43554/metabolic-activity-postmortem/43556#43556 - you might find a useful answer there. Full disclosure: top answer is mine.

You might be better asking how we define and determine death.

To rephrase @John's comment, you might be better asking "What are the most common ways we define death?"

From the deleted answer of Kawin M came this link to Quora

Ok. So when a doctor declares a person dead, it is when their heart or brain is totally not working, and won't start working no matter what they do.
This is legal death.
If your heart stops cold, you are clinically dead. This is reversible, if you are lucky. This definition basically only exists so people can say they "died". It has no real biological significance, except for the fact that your heart is not pumping blood and providing you with oxygen. This will cause...
Biological death:
Within 5-10 minutes at room temp you have reached the event horizon of biological death. Biological death is real death.
Once this time threshold is crossed, there is almost always no going back.
This is because Cells in the brain are destroyed by oncosis, and other mechanisms and forces far beyond me.

Can you add your sources?

@AliceD I mean, it's kind of common knowledge.


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Does brain size matters for the intelligence of an organism?
It was shown in a local TV show that larger the brain, larger the intelligence of that organism.
Does that mean if more number of neurons present in the brain canit helps in improving the intelligence of that organism?

does this answers your question?


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Neural signals amplitude
Can anyone explain me if there is a difference in amplitude of signals between extracellular recording and intracellular recording. I know that the amplitude of neural signals when an action potential occurs is from -70mV to 45mV for intracellular recording. The same results are for extracellular recording?Can someone help me?
Also, I have read a paper that refers:

Neural signals from extracellular recording are very weak (typically between 10 μV and 500 μV). As a result, amplification is needed before such signals can be processed further."

So my question is why neural signals are so weak (maybe author when he says 10μV refers to amplitude) when we know that an action potential has amplitude approximately 75mV(-70mV to 45mV)?

The edit to this post referring to signals between 10 and 500 Volts is definitely incorrect (unless you are measuring voltages in electric fish); maybe it was microvolts.

Possible duplicate of Why is extracellular measurement of action potentials so different from intracellular?

Those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).
You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).
Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of millivolts.


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Where did the term "vegetative nervous system" come from?
I am interested in the origin of the name. I am aware that Reil coined the term in the 1800s, but want to know why did he choose the term vegetative. I have not been able to find an answer to this question. Today it is called the autonomic nervous system.

"Vegetative" doesn't only mean related to plants, but has other less common meanings.

4 a (1) :  growing or having the power of growing (2) :  of, relating to, or engaged in nutritive and growth functions as contrasted with reproductive functions a vegetative nucleus
  b :  promoting plant growth the vegetative properties of soil
  c :  of, relating to, or involving propagation by nonsexual processes or methods
  Merriam-Webster

So the word "vegetative" refers to the growth/nutrition functions of the autonomic nervous system. The short answer is that he chose that word because, particularly at the time he chose it, that was an appropriate word to use to refer to the regulation of things like digestion. Since the autonomic nervous system has other functions, such as in sexual arousal, and because the term vegetative has other meanings, the term "autonomic" has completely replaced vegetative in this context.

I think its probably not about reproduction: reproduction isn't The most conspicuous work of ANS  the term ANS is supposed to be more general. Vegetative has many meanings. One of which is dull or passively existing. And i thnk the pasaive existence and pasaive cooperation of ANS is the major factor behindnaming it as such

Welcome to Biology.SE. We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give your opinion; explain why your answer is right with appropriate citations. Answers that don't include explanations and sources may be removed especially when they are a poor duplicate of an already existing answer. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] this answer accordingly.


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Why can't two different genetically species reproduce to give a viable offspring?
What is the reason that only organisms belong to same species can produce a viable and reproductively healthy offspring but organisms of two different species cannot?

What exactly do you mean by "viable" and "healthy"? Does this include being able to reproduce, or just being healthy and having the ablility to survive? Please clarify.

Viable - it should be living atleast and I meant reproductively healthy as healthy.

This question is based on a false premise and shows lack of research — there are many examples of interspecies hybrids that are able to reproduce with other hybrids and/or one or both progenitor species. These hybrids include many modern Homo sapiens, wolves and coyotes, several species of "new world" warblers, and many plants.

The short answer is that "different species" are defined as "not being able to produce viable offspring".  So the answer to your question is that it's a tautology; it's that way because that's how it's defined.  You're asking a question about words, not about biology.  If you were able to persuade people that a "species" was "anything living in the same area", then "different species" would be perfectly able to reproduce.
More specifically, there are many different definitions of "species", and you're asking a question about one particular definition, the "biological species" concept that was first presented by Ernst Mayr in 1942 in his book Systematics and the Origin of Species.  Mayr's definition is a useful one, but it's far from the only one; there are literally dozens of other definitions of "species".  See Wikipedia's The Species Problem for more information.
Still, it's worth asking why there biology does (to some extent) have "species" that don't interbreed; Mayr's definition has stuck because it is useful.  The first thing to consider is how remarkable it is that any two individuals (of the same species) can interbreed at all.  It's not the default option! There are thousands of highly specialized quirks that allow fertilization to happen at all. Males and females have to be incredibly fine-tuned to recognize each other, to have sperm and egg meet each other, to have the sperm identify the egg, to enter and mix genetic material ... the cascade is tremendously unlikely and has to be rigorously maintained.
So when it's not maintained -- when there's no selection pressure on two populations -- inevitably there will be genetic drift that will randomly disrupt this fine-tuned system. If a population of, say, voles is isolated on an island, they will continue to have pressure to be able to interbreed with other voles on the island, but if they can't interbreed with those on the mainland there won't be any consequences, and so over long enough time they'll drift and lose that ability -- just as many apes, not suffering any consequences from not synthesizing vitamin C, gradually lost that ability from random drift.
There's another side to it. Two populations in the same location may be positively selected to not be able to interbreed. Think about two groups of finches, one with small fine beaks that eat tiny seeds deep inside pine cones, and one with heavy beaks that crush and eat thick-shelled nuts. They each do fine, but they can interbreed and produce offspring that have intermediate beaks -- too thick to reach the fine seeds that one parent eats, but too delicate to crush the nuts that the other parent eats. Those intermediate offspring will die off, and both parents will have wasted their resources raising them.  Both parents would be better off not breeding with each other,  but only breeding with their own kind to produce specialized and efficient offspring. There is now selection pressure on the birds to recognize their own kind (perhaps through songs or mating displays) and ultimately to be inter-sterile, so they never waste resources on the un-fit offspring. There's a gradation of separation over time, in which the different populations become more and more distinct. Eventually, at some arbitrary point, humans start calling them "species", but that's just us, not biology.
"Species" is an important concept, but it's not special in evolution; speciation is just one aspect of natural selection, there's nothing magical about it.

Nice! Taxonomy isn't carved in stone. The nomenclature changes over time. The scientist decide that some subspecies should actually be different species, species are moved to another genus, etc. Are dog Canis familiaris and wolf Canis lupus different species? They can interbreed and produce fertile offspring.

In sexually reproducing organisms, fusion of gametes starts of the process of embryonic development.
If union of gametes between two genetically distinct species takes place, there may be two situations -

Same number of chromosomes - Though the number of chromosomes are same, during the first mitosis, their centromeres may not be arranged in the same plane. As a result, cell division cycle arrest occurs, halting further development.
Different number of chromosomes - The extra chromosomes which are not paired lead to differential tension on the microtubules which again disrupts the cell division cycle.

Description of cell division checkpoints.

But still there are mules, and they themselves are infertile.

There are numerous examples of viable interspecific hybrids, many of which are reproductively competent. Your answer seems to assume that these don't exist. Your answer also seems to be about post-zygotic inviability (rather than sterility) and provides no references or other support for either mechanism. One example — mules (and hinnies) have an odd number of chromosomes and while usually sterile they are very robust. This shows that your point 2 is incorrect (it may help explain meiotic failure in the hybrid, but it definitely doesn't prevent development of that hybrid).

@tyersome I agree that there are viable interspecific hybrids but the way the question is asked, it seemed to me that they want to know the reason why such hybrids are rare which is why i listed (simple) causes to explain it. I also agree that the factors I have listed are post zygotic ones. Truth be told at that point in 2017 I did not know enough about evolution (and I still don't).


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Multi-protein drug treatments
Apologies if this an obvious question - I am very new to this. I am, as of now, under the impression that multiple SNP variations interact to create multiple mutated proteins, which ultimately results in a variant phenotype.
I am wondering if the standard method of treating is this is by creating a drug that has a combination of all of the non-mutated versions of the proteins, or if drug makers simply use the protein that they believe has the biggest impact?
Thanks for the help!

Proteins are long strings of amino acids.  Drugs are generally not proteins; they are small molecules.


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Does the amplitude of action potentials vary among species?
I would like to ask if the amplitude of action potential in animals(for example zebra finch or other bird) differs from the amplitude of action potential in humans which is approximately 70mV.

I would like to note that the 70mV you're referring to, is actually -70mV, and represents the resting potential of an adult, vertebrate neuron. When an action potential occurs, the depolarization amplitude is not 70mV, but instead right around 100mV.

Does the amplitude of action potential in animals differ from the amplitude of action potential in humans?

Surprisingly, they don't!
The current model that's used to describe biophysical neurons is the Hodgkin-Huxley model, and one of its fundamental assumptions is that, action potentials (APs) are electrical events consisting of a large transient change in membrane polarization (typically around 100 mV). (source)
The reason for this can be seen when quantifying the absolute value of peak conductance during an AP, specifically when considering the average membrane resistance with respect to peak conductance. The following graph is from the original publication by Huxley & Hodgkin, just here, and it illustrates this principle.

This model applies to virtually all excitable cells, and therefore, AP amplitude values aren't specific to the organism. Consider the following table which lists AP measurements amongst various animals, and pay notice to the values in the highlighted column. As can be seen, amplitude values remain fairly consistent across all animal types, hovering right around 100mV. (source)

And then, regarding humans, just as you stated, the resting potential of a neuron is ~ -70mV. When excited, the membrane potential rises to ~ +30mV.

Most cells in the body make use of charged particles, ions, to build up a charge across the cell membrane. ... The exact value measured for the resting membrane potential varies between cells, but -70 mV is most commonly used as this value. ... The change in the membrane voltage from -70 mV at rest to +30 mV at the end of depolarization is a 100-mV change.

(source)

If you're well versed in math, you can directly compute the ~100mV change in membrane potential using the Goldman/Hodgkin/Katz equation, given that inter & extra cellular ion concentrations are known.

nice answer, nice links!


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Why does the insulin taken from pig when injected into humans causes allergy but not the insulin taken from bacteria?
At earlier times, insulin was injected to human patients that were taken from pigs and horses. But that caused allergy it seems.
But why is the insulin produced by the recombinant bacteria not causing such types of allergy?

Some more info here https://www.nature.com/nrd/journal/v15/n6/full/nrd.2015.36.html (fig 1 show the amino acid diffrences between human and porcine insuline)

Proteins and peptides vary across species, even if we give them the same name. Some are very homologous among even distantly related organisms, others differ even within a genus. Of course there are also variations across individuals of the same species.
Insulin from pigs and horses is pig or horse insulin. It differs slightly from human insulin because the genes that encode insulin in pigs and horses are slightly different than the genes that encode insulin in humans.
We inserted the genes responsible for producing insulin in humans into bacteria, so the insulin produced by recombinant bacteria is actually human insulin. That's why it doesn't produce an immune response.
There is also the issue of isolation and purification, and it is easier to produce very pure insulin free of other contaminants from recombinant sources than from animal sources.
That's the idea, anyways. Many humans tolerate porcine insulin just fine, and it isn't necessarily clear that human insulin is actually better (for example, this study).

To the OP: Note that the insulin from bacteria is not something the bacteria produces naturally. We have hijacked their protein synthesis macinery via genetic manipulation and specifically tricked it into making human insulin rather than whatever toxin / secretion they were making before.

@Arthur Indeed, this is what is meant by "recombinant bacteria" and that's why it's human insulin.


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How does 'phosphorylation of glucose' maintain concentration gradient in membrane transport (facilitated diffusion)?
Our book explains how glucose from the blood plasma gets inside red blood cells via facilitated transport.
It states here in the book that the glucose will be transported inside by a carrier protein. Then the glucose will be phosphorylated by ATP. The phosphorylation of glucose molecules maintains the concentration gradient. This prevents the glucose from diffusing back to the blood plasma.
Based from my current understanding, concentration only change when the number of dissolved molecules changes.
My question is, "How can phosphorylation maintain the concentration gradient if it doesn't change the number of molecules inside the red blood cell?"

Sort of a "magic trick" that biology does.
With facilitated transport, the movement is passive. That is, you have a protein that certain molecules/ions can pass through, but you aren't doing any pumping or using energy to move molecules. That means that the molecules are free to move in either direction, according to concentration (and electrical) gradients.
Therefore, assuming no influence of electrical gradients, the highest concentration a passively transported molecule can reach is equal concentration inside and out.
Chemically, phosphorylated glucose is not glucose. It is phosphorylated glucose. If you phosphorylate every glucose molecule that comes in, your internal concentration of glucose would stay at zero. If phosphorylated glucose can't leave via the same facilitated diffusion pathway, then glucose will effectively only come in via that pathway, it can't go back out. The result is that, although glucose inside can never be higher than glucose outside, the sum total of phosphorylated glucose + glucose inside can continue to rise above the concentration of glucose outside.
Of course, this step isn't exactly free, because it costs the energy of phosphorylation.


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What is this slug-like thing I found in my bed?
what is this thing I found in my bed? Squishy like a slug, mildly freaked out, help? I'm in Scotland Edinburgh

It appears to be upside down.. can you flip the creature and post another picture of it? That would help quite a bit. Thanks.

it looks like your slug-like thing could be a slug! it might av gotten in stuck to your clothes (or if you have a pet, stuck to that). but a better picture would be helpful.

It might be a "bed slug".


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What is this critter
I found this "thing" crawling across my drive way. Never seen anything like it and no one I know can identify it.
Was about 4 to 5 inches long and 1/4 wide. It move some what like a worm in that segments of it's body seemed to move to propel itself forward very slowly.
I have a video as well if that would help but it is one my cell phone. I live near Gettysburg PA.

Possibly some kind of bagworm moth, or clothes moth. Not sure if those are the same or different..

Upload your video on ezgif.com, convert it to a gif < 2mb in size, and add it to your post :)


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Can humans go to hibernation?
Like squirrel undergoes hibernation during unfavourable periods if we induced the hibernation causing pitutary hormones in the human blood stream, can humans go to hibernation?

This is unclear. You ask if we can go into hibernation, then say if we induced hibernation. Those are two different things. What exactly are you asking? If your question is, "Can metabolism slow down during times of decreased food," then please ask that. If your question is, "Can we manipulate hormones to cause metabolism slow down during times of decreased food," then please ask that.

Humans cannot hibernate. There are a number of reasons why we would not expect them to do so.
Hibernation is thought to be an evolutionary adaptation to cold temperatures, and food scarcity, (perhaps also predator avoidance). Humans evolved in tropical regions with an abundance of food, and are also considered apex predators. There was thus no evolutionary pressure.
If we were to induce sleep with the relevant pitutary hormones. Humans would likely die, if they do not have any life support.


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Estimation of cases with dominant inheritance
I am reading [1] and I didn't understand this passage:

All bilateral cases should be counted as hereditary because the proportion of affected offspring closely approximates the 50% expected with dominant inheritance.

Shouldn't the percentage be 75% with dominant inheritance?
[1]: Knudson, Alfred G. "Mutation and cancer: statistical study of retinoblastoma." Proceedings of the National Academy of Sciences 68.4 (1971): 820-823.

It depends on the genotype of P (parents). If only one parent carries the dominant allele, F1 will have the allele 50%.
D = dominant allele, d = recessive allele
P: dd x Dd
F1: Dd 50%, dd 50%


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Why is the thalamic reticular nucleus called a nucleus?
In the Wikipedia article on nuclei I read:

A nucleus is one of the two most common forms of nerve cell
  organization, the other being layered structures.

Is there a specific and plausible reason, why the  thalamic reticular nucleus is called a nucleus, even though it is - anatomically - a layer?
Has the TRN once been a somehow spherical nucleus and evolved into a two-dimensional layer? Or does the TRN play a functional role that normally nuclei play, but not layers?

The thalamic reticular nucleus (TRN) is a thin layer of GABAergic cells adjacent to the thalamus (Fig. 1).  Because of its strategic location between the thalamus and cortex, the TRN is often suggested to be important to attention and regulation of information flow between the thalamus and cortex (Lam & Sherman, 2011).
A nucleus is defined as a

[p]ortion of tissue that are compact accumulations of neurons having roughly similar connections and functions

Reticular is defined as

A fine network or net-like structure.

So reticular nucleus translates itself as a net-like accumulation of neurons.
In contrast to the wikipedia meaning, therefore, I interpret nucleus as more of a cluster of functional organizational units rather than a morphological characteristic of that cluster per se.

Fig. 1. Thalamic reticular nucleus. source: Dana Foundation
Reference
- Lam & Sherman, J Neurosci (2011); 31(18): 6791-9

Thanks for the clarification. But this makes things terminologically difficult:  applying - maybe unreflectedly - anatomical terms to functional concepts.

@HansStricker happy to help. I have attempted to further clarify the answer (last sentence). Also note these kind of questions are welcome over at CogSci too. Up to you.

My question stated otherwise: In which respect is TRN a "portion of tissue that is a compact accumulation of neurons having roughly similar connections (what to?)"? And don't have the neurons of a layer have roughly similar functions?

@HansStricker This is a good question (I promise I don't hate you, I just don't like some of your questions). The distinction that the Wikipedia article makes is between "layered structures" and "nuclei", not between "layers" and "nuclei". Thalamus is not a layered structure; the cells are clustered into nuclei, not into laminae like cortex or cerebellum. There isn't any structure consisting of just one layer that is thought of as "layered", you really need at least 2 layers to be layered. TRN projects inhibitory connections into the rest of thalamus.

Also you should note that in general, most anatomical terms for the brain far predate knowledge about their functions. If you want to really dissect out (pun intended) the reasons for the names of everything you are risking some level of insanity, unless the curiosity interests you. Some nuclei are named by color, some by what they happen to be under even if they are completely unrelated, some are named from an almost imperceptible similarity to sea creatures.

@Bryan: Thanks for your kind and helpful comments. I do appreciate them.

Obviously, I didn't read the Wikipedia article on nuclei carefully enough. Anyway, it was great to get some learned opinions. In the Wikipedia article on reads:

The term "nucleus" is in some cases used rather loosely, to mean
  simply an identifiably distinct group of neurons, even if they are
  spread over an extended area. The reticular nucleus of the thalamus,
  for example, is a thin layer of inhibitory neurons that surrounds the
  thalamus.


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Is O4I2 sufficient to reprogram cells (ie induce pluripotency)?
Is exposure to the chemical O4I2 (ethyl 2-((4-chlorophenyl)amino)-thiazole-4-carboxylate) sufficient to reprogram an adult cell back to pluripotency?
They sell this chemical online for pretty cheap. My question is, if I wanted to start a colony of induced pluripotent stem (iPS) cells, would I only need to buy this or are other reprogramming materials required?

No, the chemical O4I2 (thats a name, not a chemical formula btw) only helps to induce production of the Oct-4 transcription factor. Even if just this chemical is sufficient to express Oct-4 (which it might not be, I'm not really sure about that), you still need to induce transcription of other genes (usually Sox, cMyc & Klf4) to obtain iPS cells.


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Genetic engineering for experimenting at home?
I am just wondering whether it is possible to carry out small scale genetic engineering at home, without any sophiscated tools.
Ive searched google and found this http://explorebiotech.com/the-7-important-molecular-tools-used-in-genetic-engineering/
So i am wondering whether these tools are easily acquirable and how feasible it is to be done at home maybe as a hobby.
Also my budger is probably about 200 USD so my hopes arent that high.

FYI the thermocycler in your link is almost 4,000 USD. It's a Sensoquest Labcycler model. Lab consumables like plasticware can also be quite expensive (around $2 per 6/24/96-well plate, cases often come with 50-100).

Doing genetic engineering experiments at home is generally referred to as either "biohacking" or "DIY Bio". There's a number of forums out there filled with hobbyists who are doing that sort of work in their homes and garages, and discuss how to do such things in a hobbyist environment. With those terms (and the info in the Wikipedia article), you can probably find those forums on the internet. (Suggestion: look for ones where the regulars emphasize safety and appropriate conduct - not only is it better for you, it's a sign that the regulars know what they're talking about.)
However, 200 USD might be a little small to set up a decent (and safe) "biohacking" space in your own home. Possibly a better bet is to see if you can find a local "makerspace" which has a biology component. Makerspaces are places where, for a small fee, fellow enthusiasts pool together to purchase equipment (and space) to do various projects. Most makerspaces are geared toward the computational/mechanical (e.g. building robots), but there are some out there which have biotech equipment. Your mileage may vary, though, and you're likely to have more success in finding a decent makerspace in a large city than in a small town.
A final caveat is to make sure you research your local laws to figure out what is legal in the jurisdiction you're living. Especially with laws targeting illegal drug production, there are locations where possession of basic scientific equipment by normal homeowners is criminalized. There's also regulations about waste disposal and material storage that you'll need to follow. Also, in most jurisdictions accidents/damage from home labs are penalized much more harshly than, e.g., cooking accidents. Know what's legal/illegal in your jurisdiction (and by your homeowner's insurance) before attempting to set up a home lab.

There are also dedicated 'Biohckspaces' (well, there is at least one in London)

How much would you reckon I will have to spend for decent equipments etc if there isnt any markerspaces around me.

@user35897 That depends heavily on what you want to do and how "DIY" you're willing to get. For example, you don't need a thermocycler to do PCR. All you need is three heat baths at the appropriate temperature and a lot of patience. And they don't have to be "official" heat baths - you can rig something up with heating elements and thermostats. -- That's why I suggested the dedicated forums. They have the knowledge and experience to walk you through "on the cheap" options that fit your DIY comfort levels. (Which is not something that really fits StackExchange's Q&A format.)


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Hopfield-like neuron assemblies
There seems to be general agreement that theoretical Hopfield networks (consisting of artifical neurons, namely McCulloch-Pitts neurons) are biologically rather implausible, among other reasons because of their (rather strictly) symmetric synaptic weights. On the other side, some authors claim that there are neural assemblies in the brain that qualitatively behave like Hopfield networks, i.e.

they are strongly interconnected
they synaptically store a limited number of (activity) patterns
which they reach as attractors when fed with noisy or incomplete input patterns
they "learn" (mainly) by the Hebb rule

The system of hippocampal CA3 neurons is suggested to be one such assembly.
My questions:

Is there an agreement among experts that hippocampal CA3 neurons really behave similar to a Hopfield network?
Which other assemblies (possibly nuclei?) are believed to behave similar to a Hopfield network, too? (Some examples would be welcome.)

For the benefit of others coming across the question, could you include a brief explanation of what a Hopfield neural net is?

"Is there an agreement among experts that hippocampal CA3 neurons really behave similar to a Hopfield network?" - The difficulty with such agreement is that behave similar is very non-specific. Probably no expert will say either CA3 behaves nothing like a Hopfield network, nor CA3 behaves totally like a Hopfield network; rather, in some (perhaps many) circumstances or for some functions, Hopfield networks are sufficient to replicate CA3-like behavior.

I think it really depends on the level of detail and accuracy needed.
Giving a quick look on Google Scholar, it appears that indeed there is (or at least was) a belief that hippocampal networks could be reasonably modelled by Hopfield networks (e.g. see Neuromodulatory control of hippocampal
function: towards a model of Alzheimer’s disease by Menschik and Finkel, and its references). However, many of these papers are somewhat old (though this certainly does not invalidate them!) and computational neuroscience moves fairly fast.
So yes, to a certain extent, after reading some papers that corroborate it, it might appear that some macroscopic behaviour of CA3 neurons can be reproduced by Hopfield networks.
That being said, in more recent works, I have personally never seen anyone model biological neurons with such simple neurons, when cellular level accuracy is required (often it isn't). At least stochastic Hodgkin-Huxley or integrate-and-fire, for instance, are used, even if as point processes (so that it is a system of ODEs/SDEs, not PDEs/SPDEs). Even the neurons used in today's deep neural networks (which make no effort towards biophysical plausibility) are (or at least can be) more complex than sigmoiding a linear combination of inputs!
Also, for slightly larger scales, as you note, the connectivity structure is extremely unrealistic. (Just look at the histology!)
So anyway, it depends on the goal. For simple macroscopic, qualitative similarities it may suffice. But if the goal is biophysical accuracy of simulation then I would look at newer papers and see what they do.
Check out Synaptic mechanisms of pattern completion in the hippocampal CA3 network by Guzman et al.
As for your second question, just searching for papers on Hopfield networks finds a number of them. However, they appear to be largely computational or mathematical, rather than neuroscientific modelling papers.
Maybe others can find better ones though!
Disclaimer:
I am not in the field of hippocampal modelling nor have I worked much with Hopfield networks, so take my thoughts with a grain of salt.
My suggestion is to do an extensive literature search, and post what you find as an answer here :)


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Why repolarization in ventricles start in last area which is depolarized "epicardium " rather than first area "endocardium"
About ventricular repolarization , l know it start in the last area which is depolarized ( that is why it has positive deflection on ECG ) but the question is why it start in that area ( epicardium ) although l think it can begain in first area depolarized "septum and endocardium" ?
- I heard answer about blood supply is differ because period of contraction is more in the "endocardium" than in"epicardium" which will generate high pressure inside ventricles that decrease coronary blood flow then slow repolarization phase ! If this true So how blood flow can effect repolarization ?

It isn't at all clear to me what you are asking. Also, "cardiophysiology" is not helpful as a title, your title needs to include your question or at least something close to a question.

I added some information and l hope you understand what l'm asking for .

Possible duplicate of Why is pericardium muscle repolarizated earlier than endocardium?


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What is the degree distribution of synapses per neuron in the human brain?
I believe the mean number of synapses per neuron in the human cortex is around 6000.  What is the distribution around that average, either for the cortex or for the whole human brain?  E.g., is it normal, power law, etc.?

For a given class of cells, I'd expect it to be roughly normal, possibly gamma, but the distribution across all neurons is likely to be somewhat polymodal. You have extreme cases where there is effectively only 1 synapse, for example, and cells vary greatly in size both across and within brain regions. It's certainly not power law.


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Do there exist T helper memory cells?
I'm translating a Russian text touching upon the IL-17 interleukin family, and it has a kind of typo in it. I'm not sure:

As mentioned above, IL-17 was found to be expressed at the highest levels by CD3+ Th17 cells. However, subsequent studies showed that it may be produced as well by stimulated CD8+ memory T cells, γδ T cells, Th memory cells (?) and NKT cells.

The Russian text says "Th memory", there is no "cells" there. It might be a typo.
I've read a little about T cells and became curious. Are there T helper memory cells, or does being a T helper cell exclude the possibility of being a memory cell as well?
P.S. The original Russian sentence is

Как уже было сказано выше, наибольшей экспрессией ИЛ-17 характеризуются CD4+ Th17 лимфоциты, однако последующие исследования установили, что стимулированные CD8+ Т-лимфоциты памяти, γδ Т-клетки, Th памяти и популяция NKT также способны к его продукции.

Relevant: https://www.ncbi.nlm.nih.gov/pubmed/18825747

Also relevant, and open-access: http://onlinelibrary.wiley.com/doi/10.1002/eji.201343751/full

Yes, T cells -- including T helper cells and cytotoxic T cells -- form memory cells.

CD4 memory T cells: what are they and what can they do?
Origins of CD4+ effector and central memory T cells
Immunological memory
Control of innate immunity by memory CD4 T cells


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is this an insect?

The creature is about 1 1/2 inches long and about 1/4 inch at its thickest point. It appears to have six leg. It also appears to be covered in fur. It seems to have four eyes, two facing forwards and one at either side of its head. The head is snake like in appearance. The tail is able to wrap itself around things; it was hanging by it from a leaf. The creature was found in a garden in the North East of England.

Looks like you have a caterpillar.

That is a moth caterpillar which belongs to the species Deilephila elpenor, and is commonly referred to as an "elephant-hawk moth". They're fairly common throughout England and Ireland, and, according to Wiki, this would be the most appropriate time of year for you to see the caterpillar form (larvae) of this moth.

In most of their range, the adults are seen from May to July and the caterpillars from July to September, when they pupate.

With today's date being August 21st, that matches perfectly.
Also, you mentioned, "It seems to have four eyes, two facing forwards and one at either side of its head. The head is snake like in appearance".

When startled, the caterpillar draws its trunk into its foremost body segment. This posture resembles a snake with a large head and four large eye-like patches. Caterpillars are preyed upon by birds, but these shy away (at least for some time) from caterpillars in "snake" pose.


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A fish with 3 paired fins
Many species of fish have 2 or 4 fins combined into pairs. But is there a fish with 3 (or even more) paired fins? Or has it ever existed in the past?