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ATP Hydrolysis to AMP in the Urea Cycle. What is the Free Energy Change?
How is the hydrolysis of ATP into AMP and PPi in making arginosuccinate equivalent to the hydrolysis of 2 ATP?

Please provide a source for the statement you are querying. This will provide a context for us to interpret it and provide an appropriate answer. @user1136 had provided a comprehensive quantitative answer, but I wonder if your original source is making a more general qualitative point. At the moment your question is unclear and is likely to be deleted.

The answer, I reckon, is that as stated it isn't.
However,the hydrolysis of ATP to AMP and PPi yields considerable more free energy than does the hydrolysis of ATP into ADP and Pi.
That is, the free energy change for the hydrolysis of  ATP into AMP and PPi is considerably more negative that that for the hydrolysis of ATP into ADP and Pi and for the hydrolysis of ADP into AMP and Pi.
If we consider the the free energy change for the reaction ATP  = AMP + 2 Pi  (where, say, the pyrophosphate (PPi) produced by  argininosuccinate synthetase is broken down by a  pyrophosphatase), then  it is the equivalent to  the  hydrolysis of 2 ATP to ADP and Pi and (more or less) to  the hydrolysis of 2 ADP to AMP and Pi.
When dealing with ATP hydrolysis, we must take the 'chemical environment' of the phosphate group into account, not only in determining whether the bond is 'high energy' (in the Lipmann sense) or 'low energy', but also when considering the amount of free energy released by hydrolysis of a  'high energy' linkage: not all pyrophosphate linkages yield the same free energy on hydrolysis.

Cleavage of the 'inner' pyrophosphate linkage in ATP (to give AMP and PPi) 'releases' considerably more free energy than cleavage of this linkage in ADP (to give ADP and Pi).
Cleavage of the 'inner' pyrophosphate linkage in ATP  (to give AMP and PPi) releases considerable more free energy than the cleavage of the 'outer' pyrophosphate linkage (to give ADP and Pi).

If  one 'unit' of free energy is considered to be about 32 kJ mol-1 then:

The hydrolysis of ATP to ADP and ADP roughly releases 1 unit
The hydrolysis of ADP to Pi and AMP roughly releases 1 unit
The hydrolysis of ATP to AMP and PPi roughly releases about 1.4 units
The hydrolysis of PPi to 2 Pi roughly releases about  0.6 units
Hydrolysis of ATP to AMP and 2 Pi roughly releases 2 units.
Hydrolysis of AMP to adenosine and Pi roughly releases 0.4
units.

The question posed by the OP may now be answered as follows.
Hydrolysis the inner pyrophosphate linkage of ATP (to give AMP) rather than the outer linkage (to give ADP) provides a 'thermodynamic pull' of 0.4 'free energy units' to the  argininosuccinate synthase reaction.  If the  PPi is hydrolyzed by a pyrophosphatase an extra 0.6 'free energy units' are obtained and the free energy change for the combined reaction (that of argininosuccinate synthase and the pyrophosphatase) is equivalent to 2 'free energy units' (about -70 kJ mol-1).

As pointed out by Frey, & Arabshahi (1995), hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ATP, rather than the $\beta$,$\gamma$ linkage, is a common strategy in biosynthetic reactions.  To quote the final line of this paper: Cleavage of the $\beta$,$\gamma$-phosphoanhydride bridge in ATP takes place in metabolic reactions in which a smaller driving force is required.
A Small Piece of History
It was not always accepted that the hydolysis of ATP to AMP and PPi proceeded with a more negative free energy than for the hydrolysis of ATP to ADP and Pi.  To quote from  Standard Free Energy Change for the Hydrolysis of the $\alpha, \beta$-Phosphoanhydride Bridge in ATP , by Frey & Arabshahi (1995).

It  appears to be common knowledge in biochemistry  that the standard free energy change $\Delta G^{'o}$ for the hydrolysis of ATP to AMP and PPi is -7.7   to  -8.4 kcal  mol-1 [-32 to -35 kJ mol-1].  Most textbooks of biochemistry  list  values  in  this  range (Zubay, 1993; Lehninger et al.,  1992; Garrett & Grisham, 1994; Voet & Voet, 1990; Matthews & Van  Holde, 1990). Moreover, many  textbooks  also  list  the standard free energy  for  the hydrolysis of  PPi as  $\Delta G^{'o}$ = - 7.9 to  8.0 kcal  mol-1.  [-33 to -33.5 kJ mol-1]. However,  the  true  value for pyrophosphate  hydrolysis is significantly less negative (Flodgaard & Fleron, 1974). Therefore, the standard free energy change for the hydrolysis of ATP to AMP and PPi must be more negative  than 8 kcal  mol-1 [ 33.5 kJ mol-1]  as is explained in this paper

This reminder should not have been necessary.  The correct value for the free energy change in the hydrolysis of ATP to AMP and PPi is given by Schuegraf et al (1960)  , a paper co-authored by Sarah Ratner
The hydrolysis of UDP-Glucose
$\Delta G^{'o}$ for the hydrolysis of UDP-glucose to UMP and  glucose-1-phosphate is about - 43 kJ mol-1 (- 10.3 mol-1) [Frey, & Arabshahi, 1995], also considerably more negative that that for the hydrolysis of ATP into ADP and Pi
Specifics

The standard free energy of hydrolysis ($\Delta G^{'o}$) of the $\alpha$,$\beta$-phosphoanhydride of ATP to give AMP and PPi is about - 45 to -50 kJ mol-1

The standard free energy of hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ADP to give ADP and Pi is about -30 to -34 kJ/mol

The standard free energy of hydrolysis of the $\beta$,$\gamma$-phosphoanhydride of ATP to give ADP and Pi is about -32 to -36 kJ/mol.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

(For a diagram illustrating the  nomenclature of the $\alpha$, $\beta$ and $\gamma$ phosphates of ATP, see here).
Notes

Following Alberty (2000), all equations are written as 'biochemical equations' where everything is balanced except hydrogen ions.

$\Delta G^{o'}$ for the following reaction is about -50 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= AMP +PP_i $$

[1 ]  Frey, & Arabshahi (1995) give a value of -45.6 kJ mol-1 (-10.9 kcal mol-1).
[2] Dixon et al  (2000) give a value of  -48.5 kJ mol-1 (-11.6 kcal mol-1).
[3] Schuegraf et al (1960)  give a value of  -43 kJ mol-1 (-10.3 kcal mol-1).
[4 ] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -50.2 kJ mol-1 (-12.0 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -36 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= ADP +P_i    $$

[1] Frey, & Arabshahi (1995) give a value of -32.6 kJ mol-1 (-7.8 kcal mol-1).
[2] Rosing & Slater, 1972 give a value of -31.5 kJ mol-1 (-7.53 kcal mol-1).
[3] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1 ) of -36.6 kJ mol-1 (-8.8 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -34 kJ mol-1 (-8.1 kcal mol-1)

$$ ADP + H_2O= AMP +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -34.04 kJ mol-1 (-8.13 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -71, kJ mol-1 (-16.9 kcal mol-1)

$$ ATP + 2 H_2O = AMP + P_i  + P_i$$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -70.68 kJ mol-1 (-16.9 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -13.7 kJ mol-1 (-3.3 kcal mol-1)
$$ AMP+ H_2O  =  Adenosine  +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -13.74 kJ mol-1 (-3.28 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -20.5 kJ mol-1 (-4.9 kcal mol-1)

$$ PP_i + H_2O= P_i +P_i $$

[1] Frey, & Arabshahi (1995) give a value of -19.24 kJ mol-1 (-4.6 kcal mol-1).
[2] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -20.5kJ mol-1 (-4.9 kcal mol-1)


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Why do lips heal fast
Whenever I have any cut in my lips ,it gets healed in 2-3 days so why do lips get healed faster as compared to other body parts?

According to this article:

Wet or moist wound treatment significantly reduces the time required for re-epithelialization

Since the lips are (normally) constantly being moistened by saliva, this could be the reason you experience accelerated cut healing.

source: Stack Exchange

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sort: votes


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New speciations among Darwin's finches
In this video it is claimed that Darwin's finches arrived at Galápagos Islands just a few hundred years ago. Have there been new speciations over the past 200 years?

According to oneZoom.org (see the node of interest here), the large ground finch and the large cactus finch share a common ancestor about 170k years ago. Looking among Darwin finches on oneZoom.org, I could not find a more recent speciation event. I could not find their references for their estimates though.
However, part of the difficulty here lies in the exact definition of species one is willing to use (see this post). While it is not reported in oneZoom.org, grant and grant (2009) reported an evidence of reproductive isolation within the G. fortis species.

Speciation, the process by which two species form from one,
  involves the development of reproductive isolation of two divergent
  lineages. Here, we report the establishment and persistence
  of a reproductively isolated population of Darwin’s finches on the
  small Gala´pagos Island of Daphne Major in the secondary contact
  phase of speciation. In 1981, an immigrant medium ground finch
  (Geospiza fortis) arrived on the island. It was unusually large,
  especially in beak width, sang an unusual song, and carried some
  Geospiza scandens alleles. We followed the fate of this individual
  and its descendants for seven generations over a period of 28
  years. In the fourth generation, after a severe drought, the lineage
  was reduced to a single brother and sister, who bred with each
  other. From then on this lineage, inheriting unusual song, morphology,
  and a uniquely homozygous marker allele, was reproductively
  isolated, because their own descendants bred with each
  other and with no other member of the resident G. fortis population.
  These observations agree with some expectations of an
  ecological theory of speciation in that a barrier to interbreeding
  arises as a correlated effect of adaptive divergence in morphology.
  However, the important, culturally transmitted, song component
  of the barrier appears to have arisen by chance through an initial
  imperfect copying of local song by the immigrant. The study
  reveals additional stochastic elements of speciation, in which
  divergence is initiated in allopatry; immigration to a new area of
  a single male hybrid and initial breeding with a rare hybrid female.

Thanks. The second question is not much necessary to me, so I will remove it.

It is some kind of a rule though that the OP cannot just change the question (or only for mild clarifications) after someone has answered it though. You're now realizing part of the problem of why one must always restrict a post to a single question!

I would rather advice, restricting the current post to the second question only as it has already been answered (although relatively poorly answered) and open a new post for the first question.

You're right. I edited the question.

I think this article implies there have been new speciations? https://evolution.berkeley.edu/evolibrary/news/100201_speciation

I read your post about the definition of species. I was curious what's the definition of lineage, but I don't have enough reputation to comment there. Doesn't lineage refer to an individual?

From wikipedia, An evolutionary lineage is a temporal series of organisms, populations, cells, or genes connected by a continuous line of descent from ancestor to descendent. Lineages are subsets of the evolutionary tree of life Feel free to open a post if anything is unclear. I've added a link to the wikipedia page onto my answer to "How could humans have interbred with Neanderthals if we're a different species?"

I opened a new question: https://biology.stackexchange.com/questions/72521/usage-of-lineage-over-species
Not sure if it's not against the rules, since it looks kind of personal.

I think it is totally fine to cite someone (whether the cited text was published on biology.SE or anywhere else) and ask for more information. Don't worry about that

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How do plastic containers and other thrash end up in the ocean
There are many photos of the ocean, which in some parts is littered with all sorts of waste, often plastic bags, containers etc. But I just wonder - how do such large amounts land in the ocean/sea? Isn't waste disposed at secure sites - so such a bug would either be recycled or in the worst case end up on some landfill? Of course rogue companies or entities could occasionally dump some thrash into the ocean, but the massive amounts of it seem surprising to me.
Beside, often the argument is to not use plastic bags, containers etc. but simply USING them doesn't put them in the sea. So what does, and can it be stopped?

Welcome to Biology.SE. I'm voting to close this question as off-topic because it has little to do with biology! SustainableLiving.SE might accept this kind of question.

Thank you for pointing me to another Stack Exchange, I was looking for one but this one seemed most fitting. Certainly I don't intend to spam, so if there is one more suitable I am more than happy to move the question here.

I am sure you did not mean to spam. As your post has been now posted on sustainableLiving.SE (and has a good reception), you might want to delete your post here on Biology.SE.


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What is this angiosperm from Morocco?
What is this species of angiosperm? It's got succulent stems and leaves that do not produce latex. Photographed in spring.

It is a species of Carpobrotus, probably Carpobrotus edulis. However, after looking online, several of the Carpobrotus species look very similar. It is an invasive species in the Mediterranean region. See the Wikipedia link.
https://en.wikipedia.org/wiki/Carpobrotus#Species


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Requirements for ability to reproduce
In my (albeit basic) biology classes in the past, we've learned about how, to reproduce, two organisms must have the same number of chromosomes. This has been verified by a few other websites I found. So- I've heard about various genetic disorders in which people can have fewer or more chromosomes than usual. For example, if a person had tetrasomy, they would have two extra chromosomes (48 in total). Chimpanzees also have 48.
Therefore:
If, hypothetically, a person with tetrasomy and a chimp's sex cells were combined, would it create anything?
If not, what are the other requirements for creating a baby organism besides the parents having the same number of chromosomes?

You seem to be more interested in the ability to mate with another individual than to reproduce. A lot of the reproductive efforts out there does not involve any mating (asexual reproduction). You might want to clarify that in your title. Also, you might want to highlight in your title that you are interested in differences in chromosomal number among the two mating individuals.

Can you please link to the few other websites [you] found?

The ability to produce offspring has more to do with the compatibility of the chromosomes than the number. This is why hybrid species (such as mules) are able to survive (but are infertile). If you want to learn about why hybrids are infertile here is stackexchange question about.
Although, this would all be dependent on weather gametogenesis could occur with the tetrasomy. But as seen here with Down syndrome, it can be successful.


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What is this thing that is growing in my yard? And should I get rid ot if?
I live in Wilmington, Delaware (Mid-Atlantic USA).  The north side of my yard is largely shaded by my house and grass is spotty.
Periodically when I go into the yard I will find as many as four pod-like things have opened on the ground.  I almost never notice them before this stage, the one time I did it looked like a patch of dirt until I stepped on it and it sort of shattered.
I'm baffled by it and my wife thinks it's some form of fungus.
We have two children under 4 and we are concerned it could be poisonous.  It certainly doesn't enhance our yard's attractiveness.

With that in mind, I have a handful of related questions:

What is it?
Is it dangerous?
How can I get rid of it, if I so choose?

Addendum:
I believe we have found an unopened example of what we've been seeing:

It may be some type of puffball fungus.  If possible, a photo before it has opened would be helpful with identification.

@Kurt After a couple days of looking, my wife seems to have found an unopened example, I've added the photo to the question.

You might want to ask this in the gardening part of stack exchange.

Likely some kind of "earth star" fungus/mushroom. It is decomposed too much to identify.

Your wife was right--it is a fungus (hard to tell which one). There' probably a lot of organic matter under those bricks, maybe old leaves and dead wood. Location makes sense. While I would not eat it, on account of the difficulty with identification and the fact that mushrooms are often problematic, there is probably no reason to get rid of the caps (unless you have kids). Finally, even if you rip off the cap, most of the rest of the fungus is under ground. The mushroom you see (cap) is just the tip of the proverbial iceberg.

Myriostoma is a fungal genus in the family Geastraceae. The genus is monotypic, containing the single species Myriostoma coliforme. It is an earthstar, so named because the spore-bearing sac's outer wall splits open into the shape of a star. Source: Wikipedia.
But this recent article shows otherwise https://pdfs.semanticscholar.org/08ea/2ee6be93787f2e0034b85222b751a5281167.pdf

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What is this type of diagram called and how to interpret?
I'm just starting a project on neuroscience for sixth form. I have had no teaching in this area so had to teach myself entirely.
This is a "low-power image of a transverse section through
the telencephalon of an adult pigeon":

I understand the TH means tyrosine hydroxylase but I have no idea what the different colours mean.
Any information would be so helpful :)
thanks very much!

They used a stain that marks tyrosine hydroyxylase (most likely using an antibody to TH, followed by a secondary antibody tagged to an enzyme that then produces a dark precipitate in the presence of the proper precursor).
The dark regions are where more antibody bound, so you can infer this is where TH is highest. It's very difficult using these techniques to take anything quantitative from this, but you can use the technique to identify regions and possibly compare between them, given you have an appropriate control region.

Thank you so much! :) what does the white line mean?

@OllyScargill What white line?

The line up the left side of the image?

Oh the gap? I'm not super familiar with bird brain morphology but that looks to me like it's a ventricle - it's a place in the tissue slice where there is open space. It might be larger than it would be in the intact brain, because tissue tends to shrink when you fix it, but if it was perfused well there may have been minimal shrinkage.

Thank you so much Bryan :) You don't know how much you helped me out!


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What is this flat dry stick-like leaf that rattles?
I googled those terms but came up empty, here are three photos with a ruler for scale:

The hole and scratches are my dog's teeth, so as you can tell, it is strong yet not brittle. When you shake it, it rattles, like maybe there are seeds in there.
It's from a public irrigated park in a Northern Hemisphere hot desert climate (BWh) region, and I picked it up today, so spring time if that will help.
My dog is usually the one to find it, and we play fetch with it.

I believe this a seed-pod from an Inga or Delonix plant.
Inga are native to South America, while Delonix are native to Madagascar. But they've been introduced to other places and I've seen similar plants in the northern hemisphere. Inda and Delonix are both members of the subfamily Caesalpinioideae. I found the name by searching for "seed pod shaker". Sometimes you just need to know what terms to google.
Shown in the image below is pacay, or Inga feuillei.

But your pod could also be from the flame tree, Delonix regia.

It is a large seed pod of a leguminous tree (Fabaceae family).  This is one of the largest plant families that there is, so it is impossible to identify the species exactly without more information.  Many trees of this family are drought (desert) tolerant as you mention BWh region of northern hemisphere. The seed pod in your photo looks very much like Delonix regia. A couple of links are below.
https://garden.org/plants/photo/125733/
https://en.wikipedia.org/wiki/Delonix_regia


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Biological siblings possible with <9 months age difference?
I'm currently in the middle of writing a story, and one of the story elements threw up a question for me. In this story, there are two siblings, who are only one or two months apart in age. As they grow older, they start to question how this age difference is even possible. How could their mother have had another child after just a month of giving birth to the first child? They suspect that they're not related and don't actually have the same mother, and it turns out that it's true.
I want to know if that suspicion is justified. I began to think of ways two siblings can be less than the usual nine months apart in age and yet still be related to each other. One idea I had was of twins, one of whom is born earlier, while the other had to stay inside the womb for another month for whatever medical reason.
Basically, my question is: can you have siblings (with the same mother and father), who are less than nine months apart in age? And if yes, how?

If you are going into science fiction, you can look into the Twin paradox – both born at the same time, but one aged faster. Works also with "normal" siblings.

They could be 24 weeks (maybe 22 or 23 weeks) apart if the younger one was born prematurely.

They could be born at the same time, fraternal twins are a thing.

One sibling could be born to a surrogate mother using DNA from the same mother and father as the other twin.

Maybe there was a calendar reform between the two births and they forgot about that?

If this was the literature SE I would ask how these people know they're only 2 months apart, or why anyone would try to set them up as siblings without lying about their birth dates. Fraternal twins would be a very likely option if they are between 1 and 4 years old, and adding an arbitrary year to one characters fake age would be equally easy beyond this range. A typical baby only grows 2 or 3 inches in their first two months... it wouldn't be hard to tell them they're twins.

Would you accept artificial insemination as a method -- if so, two women could be impregnated using the eggs from a single woman.

What do you mean by siblings?
If by siblings, you accept cases of individuals having the same father but not the same mother, then of course, it is possible! Below, I will assume you are referring to full siblings (eventually twins).
Age gap between twins
According to the huffingtonpost, there is a case of two twins that were born 87 days apart. On average, the age gap between two twins is rather of the order of 15 minutes (Rayburn et al., 1984).
Cousins that "look like" full sibs
Imagine family A has a pair of homozygotic twin daughters. Family B has a pair of homozygotic twin sons. If the sons of family B mate with the daughters of family A, then the offspring will be cousins but will have a relatedness of two full siblings.
One can of course extend this kind of crazy scenario to any number of generations apart.
Superfetation
I discovered the concept of superfetation in @froimovi's answer. From wikipedia

Superfetation (also spelled superfoetation and superfœtation – see fetus) is the simultaneous occurrence of more than one stage of developing offspring in the same animal. It is not believed that it occurs naturally in humans. There have been 10 reported cases of possible superfetation in humans.

As @1006a rightly pointed, the two babies might well be delivered during the same labour though. If they are delivered during the same labour, then they will have the same age counting from birth but different age counting from the time of fertilization.
Uterus didelphys
See @Bakuriu's answer!
Human intervention
Other alternatives would require some human intervention. For example, fertilization could have happened in vitro and the eggs were implanted in two different wombs. One womb could be a surrogate mother and the other one could be either another surrogate mother or the woman who actually donated the ovules.
Plenty of cloning techniques could yield two full siblings to be less than two months apart. Also, techniques of ex utero pregnancy could be used (although I am not sure we have the technology ready for that). Note that human cloning is illegal in many countries.

Obviously I meant two siblings who have the same mother and father, but I added the clarification anyway. I was mainly looking for natural ways on how this could happen. The cousin one seems like cheating, though. :P

"Note that human cloning is illegal in many countries.", the plot thickens.

@froimovi For better or worse, the stackexchange idea is to write the best answer. If you can write a better answer by combining the best two answers then that's fair game. The point is simply to help people as best we can.

One of my friends was adopted. When she found her biological brother, it turned out they were born like 3 ~ 5 months apart (sorry, don't remember exact number), but genetic tests strongly suggests they are full siblings. Go figure. @noClue if you just left it as a mystery in your story, it will be good enough for me.

Yes, this can happen in non-twins. There is a rare phenomenon that can occur in humans (and some other animals), called 'Superfetation'. This is when some time during pregnancy, a woman has a second oocyte fertilized and implanted. This event is an entirely separate conception, and results in two fetuses of slightly different ages in the womb simultaneously. There are only ten cases of this in medical literature.
Here is a link to the abstract of a review on the subject.
Perhaps you can discuss this possibility in your story.  : )
https://www.ncbi.nlm.nih.gov/pubmed/18667283

Interesting. If i could pick two answers, I would. Have an upvote instead.

But note that both babies would likely be delivered during the same labor, so the birthdates would be the same. This is probably the biggest danger of superfetation—the younger "twin" may be premature, even though the overall pregnancy is full term.

@1006a But the first could be delivered through c-section to avoid this problem.

I have known kids who were 7 months apart in age - the younger one was a premature birth.  No human intervention or other special circumstances required.

This is the simplest and most straightforward answer. I'm sure this happens more often than many people would think.

@Cascabel Yes months...7 weeks would be incredibly far from viability.

@BryanKrause I simply missed "younger" and thought this was talking about twins born at different times as many other answers were (in which case a 7 month gap is not particularly feasible).

I'm not sure where pojoguy lives, but I can confirm that I've also met a mother of two boys who were born (from her womb) 7 months apart.

It's quite possible. Consider a couple who has problems conceiving children, so they get a surrogate mother who carries the couple's child. And six months later, with the psychological pressure gone, the couple conceives a child naturally. So you can have natural siblings, almost any time apart.

Why posting an answer that has already been suggested in my answer (see under Human intervention)?

Women with uterus didelphys have two different uteruses, and hence can be pregnant with two sons at the same time. The time of fertilization for the two uteruses can be different.
The wikipedia page also mentions cases of different birth dates for the children. There was a case where the births were 72 days apart.

And on top of that uterus didelphys is a rather common malformation according to wiki (In the United States, uterus didelphys is reported to occur in 0.1–0.5% of women).  +1

Daughters, too, I would guess.

@Llewellyn I use the term son as a neutral, since child does not imply the fact that it is the offspring of the mother and offspring sounds demeaning to me.

@Bakuriu I'm guessing this is a language barrier. :) In English, son simply means "male child", daughter means "female child", and child just means "someone's son or daughter". Other languages might use different words when talking about a woman's child or a man's child, but in English the parent's gender doesn't matter. (I hope I haven't offended you. I certainly didn't mean to, but I don't know how to explain it differently either. I fully agree that offspring would be a bad choice.)

@Llewellyn I can't speak for Bakuriu, but I think you've misunderstood them. As a native English speaker, I totally agree that 'son' carries much more reference to belonging to a 'parent' in the sentence than the word 'child' does. Additionally, it's definitely correct in English to use a male pronoun when the antecedental gender is indefinite.     (Like you, I'm not trying to be argumentative; I just feel like there's been a miscommunication here)

@forresthopkinsa “Son” is not a pronoun.

Surrogacy. Full siblings can be born at any age separation at all.
Medical intervention. I'm sure I've heard of one (non-identical) twin being delivered early by C-section for the purposes of surgery, while the other was left intact and delivered later.
If we're only looking at genetic siblings.... If identical twins both partner with identical twins, any children conceived will be legally cousins but genetically siblings.


text:
SNR for good MRI imaging
Resolution of MRI can be improved if FOV is reduced keeping other factors constant, but this reduces voxel volume, which in turn reduces SNR. How much SNR is enough for good imaging?

WTF are you talking about?

[Old question, but...]
There is an old adage in MRI:  High signal to noise, high resolution, short scan time... choose 2.
The question of "How much SNR is enough?" can't be answered without talking about specifics, primarily, what is the scan going to be used for?
For example, a typical MS diagnostic scan doesn't really need to be too high a resolution or signal to noise as typically the lesions are large and hyperintense.  BUT with higher field scanners one is able to see smaller and smaller lesions.
If one is doing quantitative work off of an MRI scan, then it will depend on the type of quantification, algorithm etc.
So, in some ways the question is very broad and it depends, significantly, on a lot of other factors.
Doing some Google Scholar / Pubmed searches for SNR and MRI might help with specific areas you are interested in (e.g., https://scholar.google.com/scholar?hl=en&as_sdt=0%2C9&q=minimum+signal+to+noise+ratio+in+magnetic+resonance+imaging&btnG=)


text:
Why is the nucleus accumbens in that place?
This description of where the nucleus accumbens is (Ac) says that it should be near the lateral ventricle, when it is quite clearly very far away? How is this?

the region surrounding the tip of the lateral ventricle, at the ventromedial margin of the rostral pole of the medial striatum (MSt) in birds is marked as the nucleus accumbens

(from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2481519/)

Furthermore the lateral ventricle seems to be in very different places in both diagrams although they are both avian brains?
(https://avianbrain.org/papers/RevisedNomenclature.pdf figure 2)

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2481519/ figure 1)
thank you for any help :)

Please add references for the diagrams and quoted text.

references added :)

The ventricle looks in a different place simply because the first image is a transverse section whereas the second one is a sagittal section.
In the sagittal version the striatum looks very far from the ventricle because it is a quite lateral slide, more medially it would look closer to it as it does in the first figure you show.
Here you can see a representation showing also a more medial transverse section.
source: Vertebrate brains and evolutionary connectomics: on the origins of the mammalian ‘neocortex’. Harvey J. Karten. (2015) DOI: 10.1098/rstb.2015.0060

thank you very much for the clarification that was so useful :)

So in the sagittal section diagram, would you still say the Ac surrounds the tip of the lateral ventricle?

It is not visible in that figure, but is not false.


text:
What was the first known organism to exhibit muscle growth based on activity?
Being able to grow bigger muscles to match an organism's personal habits seems like a pretty nifty feature since most organs grow to one specific size, aside from some stretching.
Was this a feature as long as muscle tissue has been around? If not which species had the ability first?

It would depend how you define a muscle no? This article has an informative take on the evolution of muscles. http://www.en.uni-muenchen.de/news/newsarchiv/2012/2012_woerheide.html


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Does thyroxine increase BMR or metabolic rate?
I know that thyroxine increases the metabolic rate, but my teacher said it increases the metabolic rate, not the basal metabolic rate, the basal metabolic rate is always the same. What's the difference between BMR and metabolic rate??

The definition of BMR from wiki is :

Basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at rest.

When BMR is calculated for a volunteer some conditions are taken into account:

complete physical rest
sitting upright
at a comfortable room temperature usually around 25 centigrade
at the post-absorptive phase of digestion

On the other hand metabolic rate may be calculated even when one is exercising, at high or low room temperatures, during digestion etc. So it is more generalised.
When you are talking about thyroxine or thyroid hormones, you must keep in mind what (factors) stimulates its secretion.
One such factor is coldness.
So that definitely indicates temperatures below the 25 centigrade mark at which BMR is usually calculated.
So in my opinion it was quite prudent of your teacher to advise you to use metabolic rate instead of basal metabolic rate for the thyroxine effect description.
REFERENCE BOOK:
Biochemistry by Debajyoti Das 14 th edition
Academic publishers P-677 to 680.


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Number of DNA in a chromosome
I wanted to know the number of DNA in a chromosome.
I previously knew that there are 2 DNAs per chromosome, but later I think I saw somewhere that it was trying to imply that the number of DNA is one per chromosome.
Please clarify this

There are two DNA chains per chromosome. There is one unbroken strand of double-stranded DNA per chromosome (except during DNA replication).

There is one or two chromatids per chromosomes (depending upon the stage of the cell cycle) and there are two (anti-parallel) strands of DNA in each chromatid.
As discussed in your previous post, you are using the term DNA incorrectly which makes your questions hard to understand. You should probably just have a look at an intro course to genetics.
If you want to learn through SE posts that I highly recommend you having a look at the posts:

Chromosome and chromatid numbers during cell cycle phases
How is the diploid chromosome number maintained at mitosis?
What are homologous chromosomes?
Interpretation of picture of human chromosomes
What is the relationship between DNA molecules and the chromosomes?

Remi b, could you please suggest edits so that the question renders authentic

What do you mean by authentic. Authentic means "of undisputed origin". Editing it necessarily reduce its authenticity. Do you mean "more clear"? Just adding "molecule" after the term "DNA" would already much improve the question!


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Impact of Natural Selection on Population Size
I have conducted a lab with my IB Biology 11 class, regarding changes in allele frequencies within generations overseeing the natural selection of an advantageous phenotype. We were looking to conclude some sort of link between the changing allele frequencies and an overall changing population number of the species. Lab results saw, that as the frequency of the advantageous phenotype increased, the total population dipped and then increased after the 3rd generation. Can anyone point out any possible reasons as to why this occurred - regarding any factors at all? The image below depicts frequency of the advantageous allele vs total population.

Can you give more detail because I don't understand?  Was this an experiment or a simulation?  What was the advantageous phenotype and did you know in advance that it would be advantageous ?
In your graph, what is on the x axis and what is on the y axis?

@remi.b Can you provide some illumination?  I don't understand it.

@JohnnyToff The question is unclear to me. Your picture does not contain any axis labels, you talk about both population size and allele frequency but I don't understand what connection you're making in between them and I do not understand exactly the pattern you've observed. If you're dealing with population, it is also unclear the population dynamic before the introduction of a mutation and it is unclear whether the mutation was beneficial or deleterious. I am voting to close as unclear.

Can you add a better image with proper axis labels? Also use imgur to upload your images or use HTML (as I have edited your original post).

You should always label axes on a graph. I know it's explained in the text, but it's best practice to label your graphs to facilitate understanding of the data you're presenting.

Related: https://xkcd.com/833/

Take the following thought experiment.
A population off 100 fish, 90 red and 10 blue. On average, a red fish has 0.5 children and a blue fish has 2. This is how the population develops after each generation:

90 red, 10 blue, 100 total, 10% blue
45 red, 20 blue, 65 total, 31% blue
23 red, 40 blue, 63 total, 63% blue
12 red, 80 blue, 92 total, 87% blue
6 red, 160 blue, 166 total, 96% blue

Notice that even though the percentage of blue fish strictly increases, the total population decreases and then increases. This is because the initial population had red fish who died off before the growth of the blue fish become noticeable. I suspect that something similar happened in your experiment, although I cannot say for sure since your description of it was vague.
I also want to make it explicitly clear that having my starting population be more red than blue fish made this effect much larger, but was not necessary. Even if I started with 50 red fish and 50 blue fish, this decrease in population followed by an increase could have still happened. It would have required less clean numbers for the fish reproduction rates, which I did not want to deal with.

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


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How much arteries expand during systole?
Arteries expand during systole. By what percentage, on an average, does the arteries' diameter change during systole  with respect to diastole? Answer may depend upon type of artery i.e. elastic artery,  muscular artery, arterioles etc, you may specify the type.
This
https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.nature.com/articles/eye199419.pdf%3Forigin%3Dppub&ved=2ahUKEwjuy4_Z2rvaAhWMYo8KHXuVAfcQFjAFegQIARAB&usg=AOvVaw3L27QesaUFNIqGfkINgy-7
paper shows 3-4% change in diameter of retinal arteries, but size of the arteries is roughly 100 microns. I am more interested in arteries with diameter more than 1 mm.


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Chromosomal pair possible in metaphase - I
There is this question which was asked in my exam.
A diploid cell contain 6 chromosomes. How many possible random arrangement of homologous chromosomes could occur during metaphase-I?
 (consider that allele for only one character present on chromosome and they are in heterozygous condition.)
Options are :
i)4
ii)8
iii)16
iv)64
Answer given is : ii)8
But my answer is : i)4
My solution :
Aa       | Aa     | Aa     |  Aa
Bb       | Bb     | bB     |  bB
Cc       | cC     | Cc     | cC
Here,  1 column represents 1 possiblity.
These are the possible combinations according to me in metaphase-I.
Am i missing something?
Please tell me where am i wrong.
PS : i would have loaded the picture of my solution but it ain't getting loaded.
Sorry for any inconvenience.
Thank you. =)

The correct answer is 8 as given by the formula 2n , where n is the number of chromosome in haploid cell.
Explanation:
During prophase 1, synapsis take place as a result of which bivalents are formed. Now each bivalent can arrange itself in two possible manner ( known as independent orientation). Since in this question there are 6 chromosomes which means 3 bivalents, the possible number of arrangement is 2 × 2 × 2 = 8
The photo here explain independent orientation in a cell having two chromosome pair. You can work this out for 3 chromosomal pair as well.
Your doubt:
As far as I can understand your doubt is that arrangement one is actually same as arrangement third ( with reference to the photo). Well, it might seem like this but if you look carefully the two non homologous chromosomes are arranged in different manner in them .. relative to each other and the homologous partner. And hence the whole arrangement is considered as different arrangements and not the same.
Thus, for 3 chromosomal pair, there are 8 possible arrangement of homologous chromosomes which could occur during metaphase-I.

The answer would be 8.
The best way to explain this would be by the formula for number of possible arrangements i.e. 2^n.
As mentioned in the question, the cell is diploid with 6 chromosomes, which means that 2n = 6 implies n = 3.
So number of possible arrangements = 2^3 = 2*2*2 = 8.
If the two homologs are A and B, mom's being A1, B1, C1 and dad's being A2, B2, C2 -
The eight possible combinations are A1B1C1, A1B1C2, A1B2C1, A1B2C2, A2B1C1, A2B2C1, A2B1C2, A2B2C2.
Hope this helps.

Yes, i get that there are 8 arrangements possible in total.  But what I'm getting confused with is it says - 'Metaphase-I '. Now,  in metaphase -I : the homologous chromosomes are still together and haven't separated yet. So,  if my one pair is let's say A1B1C1 on one side then automatically on the other side of the metaphasic plate,  A2B2C2 will be present. Same method for other combinations. So,  overall only 4 combinations are possible( Am i thinking wrong?). But,  i guess,  everyone's doing the final calculation bcz i have asked 4 teachers and they all are applying the same method.

Please point out any mistakes in my thinking. Thanks!


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What is the point of inter-species specific quorum-sensing?
So apparently, according to this TED video, there is a kind of quorum sensing involving a universal, inter-species specific molecule that all bacteria secrete. Is there any evidence of bacteria being able to examine levels of other species-specific bacteria, rather than just any bacteria that can secrete that universal peptide? It just seems like its not enough to generally survey the amount of ANY bacteria in relation to that of your own species.

All bacteria is most certainly wrong.


text:
Speed of evolution
I know that evolution can happen quite rapidly in single celled organisms. How about animals? Has there been any record of new speciations over the past 1000 years? In this video it is claimed that Darwin's finches arrived at Galápagos Islands just a few hundred years ago.

Wrong about the finches.

How do you know?

Depending on just how you define "species", it can happen in about 40 years for finches on the Galapagos: http://www.bbc.com/news/science-environment-42103058

Evolution ≠ speciation. So, it is unclear which one you are interested in!  I am voting to close.

The video is a simplification of the speciation concept in order to convey principles of evolution using Darwin's finches as an example.  Very rapid speciation (obvious speciation in 1000 years or less) for animals with much longer lifespans, is probably not documented.  However, much of a potential answer to your question depends on how you define "speciations". Species is a very fluid term. When speciation is defined as major genetic changes resulting in obvious differences that distinguish two different populations, it is easier to say "yes" it can occur in shorter periods of time. For those differences to accumulate and increase to the point where animal phenotypes and genetic differences make reproduction (genetic exchange) completely impossible probably takes much longer. Here are two links that I found helpful.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC21824/
https://en.wikipedia.org/wiki/Species

The speed of evolution is controlled by three things how fast the organisms reproduces (aka how short the generation time is)(faster/shorter = faster), how large the population is (smaller = faster), and how strong the selective pressure is (stronger = faster).
If you want a list of observed speciation events you can start here and a more indepth look and a longer list of speciation here. However a list of all know examples would be very large, outside the size available for posting here.
As for the finches they arrived on the island about 2.3 million years ago based on genetic evidence, some species on the islands may only be a few hundred years old but that is very different then when the first finches arrived on the islands.


text:
Why is cholera toxin added to certain culture media?
I was reading an article [1] where they cultured SEB-1 human sebocytes in DMEM F12 + FBS + EGF + adenine + hydrocortisone + insuline as well as cholera toxin. Why is cholera toxin added to the media? Will the toxin not initiate some kind of unwanted immune response?

https://www.ncbi.nlm.nih.gov/pubmed/25647437/

It is used to generate cAMP which promotes sebocyte growth

Empirically, it can improve growth of cell cultures (https://www.atcc.org/Global/FAQs/C/C/Cholera%20toxin-541.aspx).
It furthermore has the potential to make cell populations more homogeneous by selectively binding to gm1 containing cells that can arise from spatial inhomogeneities among cultured cells. Snijder er al. Nature 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19710653)

A quick check on Wikipedia would have answered your question.

Applications
Because the B subunit appears to be relatively non-toxic, researchers
have found a number of applications for it in cell and molecular
biology. It is routinely used as a neuronal tracer.[15]
Treatment of cultured rodent neural stem cells with cholera toxin
induces changes in the localization of the transcription factor Hes3
and increases their numbers.[16]
GM1 gangliosides are found in lipid rafts on the cell surface. B
subunit complexes labelled with fluorescent tags or subsequently
targeted with antibodies can be used to identify rafts.


text:
Why does the rabies virus have such a long incubation period?
So there was a case in India, where a man developed rabies 25 yrs after the dog bite. Source:
https://www.google.co.in/amp/s/m.timesofindia.com/city/goa/25-yrs-after-dog-bite-man-gets-dies-of-rabies/amp_articleshow/16415870.cms
I have the following questions:
1) what are the reasons behind such a long incubation pd?
2) in such cases, can vaccines taken years after the dog bite save the person? (Even though it’s advised to take it immediately)

I think the article described that the virus was sequested in the tissue, and that is why it did not spread. Also I think one can do treatment after exposured although 25 years sound long. I think it depends on if the patient had been vaccinated previously as well. source: https://academic.oup.com/cid/article/30/1/4/323391

This question may not be particularly answerable.
The only available information about this specific case is in the original article (Shankar et al. Ann Indian Acad Neurol. 2012 Jul-Sep; 15(3): 221–223. doi:  10.4103/0972-2327.99728); they say only:

The anatomical site of viral latency and the mechanism of reactivation of rabies, a neurotropic virus, remains an enigma to be unraveled.

Other reports in the literature of long incubation periods (>7 years, the previously reported maximum seems to be 14 years) are scattered/old/speculative, e.g. Gavrila et al.  Ann. Inst. Pasteur 1967 Vol.112 No.4 pp.504-15:

Discussing these cases of prolonged incubation periods, the authors point out that in rabies the incubation period can vary within very wide limits and that it is possible in areas where the disease is enzootic that, in very exceptional cases, the disease can develop after an incubation period which may sometimes greatly exceed the maximal limits now admitted, and that, as for example in cats [this Bulletin, 1965, v. 62, (1106)], stress conditions and so forth may lead to the generalization of the virus until then quiescent at the point of entry.

Plotkin 2000 Clinical Inf Dis 30:1 says

the reasons for this long latency are unknown ...
   in the absence of specific prophylaxis, the virus becomes hidden, only to invade the CNS weeks, months, or years later. Where is the virus during this period? There is some evidence for slow replication in muscle cells and for latency in macrophages, but there is no certainty that these account for the long incubation periods.

There has been an experimental study on skunks (Charlton et al. Acta Neuropathologica June 1997, Volume 94, Issue 1, pp 73–77) that suggests there is some infection of muscle cells at the injection site, but otherwise not much is known about the mechanism.
I would guess that vaccination would be effective if it were administered soon enough, but it will probably be hard in these surprising cases to identify the disease soon enough.

The incubation period for the rabies virus is typically not that long - usually under 1 month.  The reasons for longer incubation period include site of virus entry (where on body the infection occurs) and the viral load (how much virus enters at the infected site). Although there are examples of very long incubation (many months or years), reasons for this are unknown.  You may find the link below helpful - see under "symptoms".
http://www.who.int/mediacentre/factsheets/fs099/en/


text:
In the induced fit model for enzyme action, does the enzyme active site change slightly after products form?
The reason why I am asking is because I am looking at a past paper and they highlight that it does. I have attached it below. Could you explain why this is the case.

I am just looking for a quick overview of why this is the case.

I understand now that they are highlighting how during the transition state the enzyme was induced to change shape, but once products formed and left active site, there was further changing of shape of the enzyme active site so it could return back to its original shape - therefore it could be reused again, as in line with the role of an enzyme/ catalyst.


text:
What exactly causes SSRIs, SNRIs, and tricyclics to induce akathisia?
Such as too high neurotransmitter levels (serotonin/dopamine/other) or the method of drug delivery or some other reason?

Please keep in mind I know very little about this subject, I apologize for the vagueness


text:
What is the difference between infected and infectious in epidemiology?
I am studying the SIR model and in the infected class I, both infectious and infected individuals are included, as stated here
I know that the model uses the assumption that the disease has an insignificant incubation period so infected individuals are capable of transmitting the disease as soon as they become infected. But what is the specific difference between these two terms? Does infective mean anything different?

(The document you link to says "see Chap. 1 for distinction between infected and infectious individuals", but I'll assume you don't have access to that - I certainly don't.)
Infected individuals have been infected by a pathogen.
Infectious individuals have the potential to transmit a pathogen to
others.
Note that the definition given for "infected" in the source you link to is actually wrong: hosts may have a subclinical infection, in which case they are not "now sick with it".


text:
Sampling of Species counting same member of species twice
As part of the biology class, we performed a sample on the number of red squirrels in a forest a few miles away from the classroom to estimate its population.
When we returned to analyse our data, we were discussing about the validity of our sample, and I was wondering whether the idea that the same member of the species being sampled twice may have an effect.
The book I was reading stated:

a sampling procedure does not have to uniquely identify each member of a population to gain an idea of relative numbers.

I'm slightly confused as to why sampling the same member of the species twice is not something that affects the validity of our final estimate for population size.
Can someone explain why the passage in the book is correct?

Can you please explain exactly how you estimate the population size. Do you do some capture-marking-recapture or some other method? Do you take any genetic data?

Note that the quote says, "relative numbers." This means that you would need to use the same sampling procedure for each sample (true but not necessarily obvious). Then when comparing samples one would expect that different samples would have similar numbers  of species being sampled twice.
In other words, as long as each sample is obtained in the same manner, one would generally expect that the same sampling errors would be replicated in each sample, and therefore would still allow one to gain "an idea of relative numbers."


text:
What species is this yellow flower of angiosperm from Morocco?
What species is this yellow flower of angiosperm from Morocco? I photographed it in spring. I estimate the diameter of a flower to be 1.5 cm.

It's undoubtedly in the genus Oxalis but there are hundreds of species in this genus.  The genus name refers to the high content of oxalic acid found in this genus.


text:
Why is the heart adversely impacted by chronic psychological stress, yet it benefits from routine physical exercise?
Chronic psychological stress is commonly said to be deleterious to the heart, and predispose one to cardiovascular disease. Yet the opposite is said about regular aerobic exercise. Physiologically, What is the difference between psychological stress and physical exercise, with respect to their impacts on heart function/health? Both involve an increase in sympathetic cardiac input, and thus more vigorously contracting cardiac muscle; but how is one damaging and the other beneficial?

That's a interesting question. If in a few days, you still haven't got an answer here, you might to give it a try on Health.SE.

they involve different hormones, I would start there, I know stress hormone damage a lot of things, not sure about exercise ones.

From the perspective of sympathetic nervous system

Exercise induced adaptations of heart

A common phenomenon in endurance athletes is the athlete's heart /athletic heart syndrome

Once athletes stop training, the heart returns to its normal size.

You must understand why this type of adaptation is happening in them:
Firstly the athletes train to produce work output at near maximal levels/ sub maximal levels of work done which cannot be physiologically achieved in a day.So the increased heart rate generated by the sympathetic stimulation is sufficient to fulfill oxygen demand of the body only at certain levels of work done by raising the heart rate
As the grade of work done nears submaximal level the oxygen demand increases in the body and the increased sympathetic stimulation (which also restricts the cardiac muscle efficiency by decreasing diastolic time,coronary blood flow) is no longer able to suffice it.Such high oxygen demand is responsible for the useful adaptations of the heart in the form of athlete's heart.Athlete's heart reduces the need for sympathetic stimulation to increase cardiac output .

During intensive prolonged endurance or strength training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time.

Comparison with chronic psychological stress

During stress the body may or may not have high oxygen demand (the principal stimulus for adaptation) because the sympathetic stimulation is psychological and not in response to physiological work.So the heart instead of adaptating gets afflicted with detrimental pathophysiological effects of prolonged sympathetic stimulation.

stressors’ contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis.

From the perspective of cortisol (stress hormone)

Effect of psychological stress on athletes

When we are talking about the detrimental effects of psychic stress it is important to note that it may override the cardiac adaptations and severely affect performance like,for example high cortisol levels in blood released in response to stress (physical/ psychological).Although cortisol levels in the blood observe a circadian rhythm in normal healthy indivituals, some reports claim that exercise reduces detrimental effects of high cortisol levels on the heart.However,stress may override exercise induced effects in athletes but this is a prospective study, subject to greater research

A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue

REFERENCE TEXTBOOKS:

Exercise Physiology And Ergonomics (An Introduction) Asis Goswami Academic Publishers.Pg-39 to 57

Essentials Of Exercise Physiology (4th Ed.) Victor L.Katch,William D.McArdle,Frank I.Katch pg-302-333

I have an answer, but it is not ideal because science's current understanding of the answer to your question is somewhat limited.
The detrimental influence of physiological stress upon the heart is thought to occur because the physiological stress causes the cardiovascular system to prepare to meet anticipated energy needs by 1) increasing pulse and blood pressure, which can cause a heart attack that immediately follows the stress and and 2) increasing the production of glucocorticoids, which are thought to cause atherosclerosis, thereby increasing the likelihood of future cardiac maladies. Why do glucocorticoid levels increase in response to stress?  That is somewhat controversial.  See this article:  https://www.ncbi.nlm.nih.gov/pubmed/10696570.
What about physical exercise?  To some degree, whether the exercise is favorable or not is dose-specific.  Comparatively moderate exercise (relative to what the body is capable of) will have a favorable effect, while exercise that is too strenuous will not.  Physical exercise also increases pulse and blood pressure, which can also cause a heart attack that immediately follows the stress.  But if the exercise is of moderate severity, there will be two sources of beneficial effect upon the heart:
1)  There is the general phenomenon by which muscle fibers become stronger in response to the imposition of stress upon those muscles, whether those muscles are skeletal or cardiac muscles.
2)  There is the phenomenon of hormesis which is characterized by a general improvement process to all cells (including cardiac cells) at the cellular level in response to many different kinds of stress, including physical exercise and caloric restriction, both of which are sources of stress that have a hormetic effect at the right doses.  Edward Calabrese has been the most prolific researcher in demonstrating the hormesis effect, but its mechanism is not well-understood.
(A difference between psychological stress and physical exercise is that I do not think even moderate doses of psychological stress offer these two benefits.)

I believe the best answer to your question is that psychological stress increases the levels of a chemical compound called cortisol in the body (a glucocorticoid stress hormone) while physical exercise tends to decrease the levels of this "stress hormone".  Of course, physical exercise also positively affects muscles and the heart in other ways, so this is another factor. The benefits of low levels of cortisol vs. the deleterious effects of high levels of it are explained and outlined at length in links below.
https://en.wikipedia.org/wiki/Cortisol#Regulation
https://en.wikipedia.org/wiki/Exercise
https://www.mayoclinic.org/healthy-lifestyle/stress-management/in-depth/stress/art-20046037


text:
Identifying a possible pathogen of a succulent plant (Haworthiopsis attenuata) presenting with small brown scales
I have a succulent (most likely Haworthiopsis attenuata) that is currently not looking so hot. I recently noticed a number of small brown scales growing on multiple leaves (Eastern USA), that I think are some sort of pathogen:

They don't appear to follow any sort of pattern like the white marks on the leaves.
They are easily detachable with tweezers--I plucked two or three off as a test.

The best explanation I've found myself is that they're some sort of scale insects, but they seem really tiny. These are about the size of a Chia seed--only a few mm across. What are these, and as a bonus, how can I get rid of them? Photos are below:

I also would say that these are scale insects. You could try brushing them with slightly soapy water. Maybe you will get better help at https://gardening.stackexchange.com/


text:
What prevents platelets from clotting regular blood vessels?
Platelets clump together to initiate clotting, but, why don't platelets clot within healthy tissue and cause heart attacks all the time?

Platelets activate when the exposed collagen (which is normally present below the endothelium) at the wound site binds to the platelets, forming a plug. Other factors are also secreted which aid in stronger binding. A signaling cascade is triggered which then makes platelets release proteins called integrins, which help for tighter binding of platelets at the site. Activated platelets also release many stored compounds from their granules which initiate further signaling cascades to form a clot.
In a healthy tissue, there is no exposed collagen. Ergo, No clotting.


text:
What does the immune system do to stop pathogens that aren't killed by macrophages?
For instance, say a host is infected with salmonella where the pathogen can enter into a macrophage without the macrophage destroying it. How does the body then fight off an infection that is capable of surviving the mechanism by which pathogens are destroyed?

what do you mean by: pathogen can enter into a macrophage without the macrophage destroying it.

You're asking for an entire course on immunology. Googling for "immunity to salmonella" turns of hundreds of answers, from detailed peer-reviewed articles to Reddit and Quora summaries.

Basically read this article and understand that an answer to this questions can boil down to Figure 1 in the paper, but comprehending Figure 1 is an entire college course. https://www.frontiersin.org/articles/10.3389/fimmu.2014.00516/full

You can also try this review for an overview of what happens when you can't clear viruses.

It definitely 100% does not take an entire course to generally explain this one single phenomena, I can guarantee that having graduated from a program in which I studied human anatomy and microbiology, so I 100% absolutely expect it to be generally answerable within the stackexchange platform. The problem is no one went into detail about this interaction with salmonella since it is less commonly studied compared to microbes like e-coli, and many sources on the internet are commercially based, but I remember a related topic being briefly covered and not at all overly complicated by any means.

There are two broad types of infection classified by their persistence: acute and chronic infections.
I find that most courses on immunology nicely cover acute infections and their detection, and resolution. In the case of S. typhi, which has the ability to invade host cells such as phagocytes and inhibit their ability to properly function, the case isn't so pretty (1). The same can be said for some viruses like HepC and HIV, or other bacteria like Mycobacterium.
Salmonella spp. have a number of virulence factors. The flagellum of the bacteria actually acts as a TLR agonist that activates phagocytes like monocytes/macrophages and neutrophils, which are often first-responders. Then, the bacteria can facilitate the injection of some of its own proteins into the host cell which does a number of things like modulate vessicle trafficking, suppress cellular functions, induce apoptosis and promote overall survival of the bacterium inside the phagocytes (2).
So normally, and referring to the below figure, the overall reponse to a Salmonella infection is adaptive in nature, presumably because your innate effectors have been stunted:

SRC
You can see in healthy phagocytes that through one of two pathways, protein antigens end up displayed on HLA molecules for cellular immunity to take over. Option B is that another cell like a macrophage detects distress signals from the infected cell and induces cell death in it through receptors or oxidative burst. In the case of Salmonella, HLA expression is down-regulated and oxidative burst can be inhibited so localized, infected antigen-presenting cells cant mount an effective response.
That's not to say everything is de-regulated early on. If you succeed in antigen presentation or innate killing (perhaps a non-pathogenic strain), you will resolve the infection as seen in the above figure: a combination of T-mediated killing, B-mediated killing, NK-mediated killing, and generalized inflammation.
In the chronic case, the pathogen will have escaped the primary immune response, but the system will attempt to continue to resolve the infection. This can lead to a number of things: cellular anergy, cellular hyperactivity, sequestration (see granuloma), chronic inflammation & tissue damage, and so forth. The following diagram is predicated upon viral infections but the immunology is largely similar:

SRC
There are changes to the system that are a result of over-exposure to antigen, and an inability to clear that stimulation. The best way to explain it is that chronic stimulation leads to both hyperactivity and suppression. The constant presence of effector molecules like TNF-a leads to a persistent state of tissue inflammation, which is bad for the tissue, but taken together with the persistent presence of antigen, this may lead to dysfunctional responses by lymphocytes (3).
A particularly virulent infection may be impossible for your immune system to clear without assistance, then, requiring the intervention of gram-negative antibiotics, for example.


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Knockout and knockdown of gene
Out of curiosity, I got this question whether knocking out (deletion) of a gene on one side and knocking down (RNAi) of the same gene on the other side will affect the cell in a similar manner or not.
If not why?
If yes, is it applied to every gene?
Knock out of a gene will correspond to no expression (gene deletion) in the cell, which can be appropriate to confirm the functional specificity, to observe processes which are affected in its absence and some other processes which are compensating the absence of the gene.
Knockdown of a gene will result in expression defect by decreasing the level of the transcript (mRNA silencing).
Now, the points which I am wondering upon are:

no mRNA presence and silenced mRNA will create two different environments for the cell to deal with or not.
whether the whole amount of transcript should be targeted to have the same phenotype as of gene knockout.

As I understand KD, it is a significant reduction of gene expression (the gene is "down"), while KO (in a homozygote/haploid organism) results in no expression of the gene (it is "out").

@abukaj This sounds like a good start for an answer. Why don't you write one?

This is a fascinating set of questions.  The only one I can comment on is: is KD qualitatively similar to KO?
My answer is: sometimes yes, in general no.  To understand why, I like to think of a hypothetical plot of "phenotype of interest" on the y axis, and "expression of gene" on the x axis.  You can imagine that this plot could be monotonic, i.e. that the phenotype continuously increases or decreases as expression increases.  Or it is also possible that this plot could have one or more minima or maxima in it.  One example of KD giving dissimilar results from KO is for essential genes.  If they are knocked out, they of course kill the organism.  However, there may be some levels of essential gene knockdown for which the phenotype is actually increased relative to wild-type!
I will selfishly share one of my articles where I observed something like this.  We found that ADH1 knockdown improves butanol tolerance in yeast, but that ADH1 knockout was highly detrimental to butanol tolerance.  http://dx.doi.org/10.1007/s10295-015-1713-7

Naively you would expect that they should have about the same effect, but in reality a lot of things can happen. Gene knockout can induce compensating upregulation of other genes and RNAi can have off-target effects. See e.g. this paper
"Genetic compensation induced by deleterious mutations but not gene knockdowns" https://www.nature.com/articles/nature14580

As I understand KD, it is a significant reduction of gene expression (the gene is "down"), while KO (in a homozygote/haploid organism) results in no expression of the gene (it is "out").
Quoting Wikipedia:

Since RNAi may not totally abolish expression of the gene, this technique is sometimes referred as a "knockdown", to distinguish it from "knockout" procedures in which expression of a gene is entirely eliminated.


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What is this pink angiosperm from Morocco?
What is this pink angiosperm photographed in Morocco in spring? The diameter of the flower is about 2 cm. The petals are fused. The plant is crawling and did not have any erect parts.

Could be some kind of Convolvulaceae

It does indeed look a bit like bindweed. I hope to get a genus.

This is a species of morning glory (fairly obvious from the flower). It is a member of the angiosperm family Convolvulaceae. The flower and the leaves together identify it as Convolvulus althaeoides. It is a Mediterranean native.  Links provided.
https://en.wikipedia.org/wiki/Convolvulus_althaeoides
https://www.google.com/search?q=convolvulus+althaeoides&source=lnms&tbm=isch&sa=X&ved=0ahUKEwit1P3t7L7aAhVPmVkKHZIJD_gQ_AUICigB&biw=1097&bih=642


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What is this plant with white-spotted thorny leaves from Morocco?
What is this plant with white-spotted thorny leaves from Morocco? Photographed in spring.

The distinctive leaves identify the plant as Silybum marianum. It is a member of the plant family Asteraceae. It is commonly called "milk thistle". Originating in the Mediterranean region, it has now spread to many places around the world.  The plant in your photo is immature at ground level. These links will give a better idea of the mature plant.
https://en.wikipedia.org/wiki/Silybum_marianum
https://www.google.com/search?q=silybum+marianum&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiG46Kj6L7aAhWvpFkKHfYjA0AQ_AUICigB&biw=1097&bih=642


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What kind of bug is it?
I really wonder what this is:

I find it near pound in Czech Republic (Central Europe). It's 2 inches long, AP. half wide. It was quite fast.

It is a Coleopteran insect (Beetle order) in the Ground beetle (Carabidae) family. Based on the elytra (protective wings) and the dark first antennal segment, it looks like Carabus granulatus. C. cancellatus is very similar, but has reddish first antennal segments. I don't think there are any other similar species in the Czech republic, but don't know the fauna there well. Overall, Carabus has many species and several are native to Eurasia and can be a size of 2 inches.
https://en.wikipedia.org/wiki/Beetle#Wings
https://en.wikipedia.org/wiki/Carabus
https://en.wikipedia.org/wiki/Carabus_granulatus
https://www.insecte.org/forum/viewtopic.php?t=160369

I agree, based on the european species I know of, it should be Carabus granulatus, C. clathratus or C. cancellatus. I suspect all of them are found in the Czech republic.

Scratch C. clathratus, which has pits between the elytra lines (instead of raised bumps). In my literature, the other two are separated by the color of the first antennal segment, which cannot be seen clearly in the picture.

I am so sorry. I wanted to do better picture, but it run away as soon as it noticed me. But I have a picture, where it can be seen (I think so). Anyway I didn't put it there in first place because don't have clue how to identify a bug in science way.

@user40760 The dark first antennal segment in your second picture says that it is Carabus granulatus. On C. cancellatus it is reddish in colour.

Sorry for the late answer. I only bumped into this photo today. And sorry, guys. It is neither granulatus or cancellatus. This is a Carabus ullrichi. Without a single doubt. granulatus is narrow and elongated. Primary and secondary keels with cancellatus are more narrow. This one is convex, plump with very distinct keels.
Carabus ullrichi. For sure.

Can you add sources to your answer, and an image showing that it is indeed this speccies?


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How do ants get oxygen in deep colonies?
With ant colonies getting to be +7 feet deep, how does oxygen renew that deep for their respiration demand?

A basic Google search returns several relevant papers, which could be a start:   nest aeration ant colony oxygen

Thank you. Obviously I tried searching google first. The connotation of your use of "basic" is belittling.

Sorry, that wasn't my intention. My point was that it was a quick search without much effort or thought on my part, that still looked useful. I didn't have time for anything else right now (or an answer), but thought that it could still be useful to get an overview, or to rephrase the question based on a bit more background. Also, if you tried searching google before asking, it is useful if you add some of what you found, and what information you are missing/found lacking.

We do expect questions to show some effort to research answer prior to posting (homework rule). so if you include some prior research you will be fine. google provides a few useful sources but not a lot. Ant have multiple strategies and it is a hotbed of research right now. keep in mind the true extent of some ant colonies was only recently discovered.


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Can you do DNA seq with Microarray?
Is it possible to do the entire DNA sequencing with Microarray or would you have to use Sanger or NGS methods for that?

Microarrays generally capture gene products, such as mRNA (via cDNA), which have been extensively processed. Because of this, you lose genetic information such as introns or regulatory elements. In fact, what you'd end up with is the transcriptome of the organism, and it would be impossible to sequence the DNA from this. NGS methods are superior for this, still, and there is a good overview of the advantages of RNAseq over microarray here, for example. To sequence the DNA you will probably use NGS.

Source: JCI


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What is this plant from Morocco?
The plant was photographed in spring in Morocco. It's an angiosperm. It is about 2 metres high and has feathered fruits. What species is it?

Looks like Nerium oleander based on the leaves and the seeds/pod.  If not that species, certainly in the genus.  This is a common landscape plant in arid environments, and native to your area according to Wikipedia.  It contains extremely toxic substances that affect the heart, called cardiac glycosides.  Consuming these substances, which are found in the white latex, causes the heart to beat itself to death.

I once heard an anecdote telling that soldiers in Napoleon's army invading Spain got poisoned using this plant to make skewers.


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What species is this bushy thorny yellow-flowered angiosperm from Morocco?
What species is this bushy thorny yellow-flowered angiosperm from Morocco? Photographed in spring in a dried up river bed. The bush is about 1 metre high.

I happened to come across a photo of a similar leafless shrub (without flowers) that also had 120 degree branches and looked thorny, or Spiny is probably a better description. It helped me to identify the plant in your photo as a Launaea arborescens. It is an unusual species of Chicory in the dandelion family, Asteraceae. Being tolerant of arid locations, it native to northwest Africa and southern Spain.
http://encyclopaedia.alpinegardensociety.net/plants/Launaea/arborescens
https://en.wikipedia.org/wiki/Launaea
https://en.wikipedia.org/wiki/Launaea_arborescens

Well done user22542!  I thought it looked "chicory-ish" but that's about as far as I got.  I've been watching this question ever since hoping someone would figure it out.


text:
What is this species of asphodel from Morocco?
It grew about 2 metres high. Photographed in spring. It has 6 tepals and 6 stamens.

It appears to be Asphodelus aestivus, but there is similarity with Asphodelus ramosus, both of which have strap like leaves and highly branched stems. They have some overlapping ranges as well in southern Mediterranean/north Africa.
https://en.wikipedia.org/wiki/Asphodelus_aestivus
https://en.wikipedia.org/wiki/Asphodelus#Systematics


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What is this species of angiosperm from Morocco?
The flowers are about 1 cm long. The plant is about 1 metre high. Photographed in spring. The plant was found in a ruderal environment.

Looks a bit like a Flax relative, genus Linum, but the hairy leaves and stems aren't consistent with Linum usitatissimum which is the flax of commerce (the textile linen).

Look into the Symphytum genus, or related genera within Boraginaceae (the forget-me-not family). It is loosely similar to Symphytum officinale, but clearly not that species. The overall layout, size, leaves and hairyness of the stalks is similar to species in Symphytum.
Here is Symphytum officinale, as an example of the overall appearance:

Also similar from the Anchusa genus in the same family (Anchusa azurea):

For the record; I don't really think this answer deserves the "accepted" badge.

I agree with Borraginaceae. The examples you provide could be close, but the leaves seem a bit different.


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Can you please identify this beetle?
Can you please identify this species of beetle? It was about 2 cm (or 0,8 inches) in size. Photo is from Greece, Europe.

Could you please add the (estimated) size of this beetle?

about 2 cm ,  0,8 inches.

It looks a bit like a Phyllopertha horticola (Garden Chafer, from Scarabaeidae), with the antenna hidden, but 2 cm is too large. It could be a related Scarab beelte though, or you are overestimating the size (which is common with insects, when you dont actually measure them). The picture is a bit dark to judge though.

Definitely a scarab, likely Subfamily Cetoniinae. You should post an answer @fileunderwater

The insect in the Photo is a beetle (order Coleoptera), in the scarab family (family Scarabaeidae). It is most likely in the Genus Phyllophaga (June or May bugs) or Phyllopertha (garden chafers).  Beetles such as this are commonly referred to as "Chafers" feeding on plant leaves and flowers during the day. One of the defining characteristics in the photo is the apparent "Hairiness" (setae) visible at the sides of the insect body. I am inclined to agree with the good observations expressed in the comments.  It likely to be a garden chafer Phyllopertha horticola. Some helpful links are below.
https://en.wikipedia.org/wiki/Phyllopertha_horticola
https://en.wikipedia.org/wiki/Phyllophaga
https://www.flickr.com/photos/72271115@N02/galleries/72157651475342046/?rb=1#photo_14184003066
https://www.flickr.com/photos/odonataman/14184003066/in/gallery-72271115@N02-72157651475342046/
https://en.wikipedia.org/wiki/Scarabaeidae


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What is the type of conservation in which seed banks are an example?
Firstly I think this question is quite ambiguous (I did not come up with it) so sorry.
I have only come across 4 'types' of conservation: environmental, animal, marine, and human conservation.
I am aware that animal conservation includes their habitats, so perhaps keeping seed banks is a way of preserving habitats.
I may generally say that seed banks are a way of preserving biodiversity but I don't know if 'biodiversity conservation' is even a thing.

I don' t really get what your "types" are referring to (do you have a reference to these specific four types?) and they are clearly not covering all cases in conservation biology. They are also not mutually exklusive, and can overlap. Also, by "seed bank"I assume that you are referring to human conservation of seeds (as genetic material, see eg the Svalbard Global Seed Vault) and not the soil seed bank that some species has.

@Mesentery could you expand?

I agree with @fileunderwater. The "types" you list are unclear. The question is based upon a series of issues of terminology and semantics and therefore cannot be answered. Anyone could just say random things like "agriculture conservation", "plant conservation", "economic conservation", "field conservation", "forest conservation", "private-sector conservation", etc... and there is no way to judge what would make sense or not. I am voting to close as unclear.

@Remi.b I am simply rewriting the question that has been set as homework. Any ambiguity is therefore not at all down to me. Part of the reason I asked here is because I did not really understand the question. I also "shared my previous  attempts" at the question and therefore have met the question asking guidelines.

@BenHughes Is there a certain book your homework/lectures is based on? Or did you get any definitions during the lesions regarding the terms you used in the question?

@Marzipanherz no it was amongst a bunch of past paper questions he set us

@BenHughes You might want to link to this series of paper. Maybe one of them attempt to do this kind of categorization.

Seed banks are a part of "plant conservation" efforts which is missing from your list.

IMO the question makes no sense and an answer to a senseless question cannot make any sense (unless it starts by redefining the question). -1

I do see your point.  But, one of the problems that I've seen on one other SE site is that questions go unanswered because they are somehow viewed as unworthy.  I choose to answer if it takes less energy than many of the comments. IMO.


text:
Why does cut grass cause allergies?
I know that cut grass from a lawn or field can cause allergies in some people.
I also know that most plant allergies are due to plant pollen.
However, most people do not allow their lawn grass to flower, and therefore, any allergy from cut grass is likely not due to pollen.
So, what exactly in the grass is causing the allergy?
I did a google search but only found evidence and info for grass-pollen allergies.
Does anyone know what's going on here?

www.allergicliving.com claims that the cause to such an allergy is not the grass but is actually mold:

Often patients will have allergy symptoms with fresh cut grass...That's not grass pollen allergy, that may be mold allergy from the molds being stirred up.

The site also mentions that simply having the physical presence of lawn mower "dust" in one's nose may cause symptoms.
Source: www.allergicliving.com/2010/07/02/outdoor-allergy-grass-allergy-attack


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HELP! How will pH 14 affect enzyme structure?
If a substance is very alkaline/ basic, e.g. a pH of 14, does this mean that there are near to zero H+ ions (or it is possible to have such a situation where there are zero H+ ions and it is still alkaline) or does it mean there are lots of OH- ions relative to H+ ions? If so, how will this affect enzyme structure in very alkaline/ acidic conditions?

pH can go more than 14, also probably better off on chemistry

I'm voting to close this question as off-topic because it is a chemistry question (see chemistry.SE) and not a biology question.

pH is most definitely a chemistry question. Acids and bases are chemistry, pH is crucial for many many chemical reactions that have absolutely nothing to do with biology. It's not much relevant to today how the idea initially spread.

This is a very chemical explanation. Here goes.
$\ce{pH = -log[H+]}$
$\ce{pOH = -log[OH-]}$
$\ce{pH + pOH = 14}$
Therefore, at a $\ce{pH}$ of $14$, $\ce{pOH}$ is zero, so there is 1 mole of $\ce{OH-}$ and $10^{-14}$ moles of $\ce{H+}$ in a liter of your substance.

Yes, in a simplistic model; although "in a mole of" should be "in a liter of".

Please do not answer (or up vote) chemistry questions on biology.SE. Off-topic is off-topic.

I don't think it's too off-topic as he said something about enzymes at alkaline environments, but it doesn't seem like he researched a lot before hand, as the very definition of pH involves the concentration of H+.


text:
Pitch perception - why is the missing fundamental not directly detected in the cochlea?
I'm learning about pitch perception, and learned about the case of the missing fundamental.
In the main image in that wikipedia page, it seems like the bottom graph, with the fundamental frequency and its second harmonic removed, that the wave is still very periodic at 100 Hz. Since the Organ of Corti has some area which should be excited when there's a sound wave of frequency 100 Hz, why does this sound wave, which seems periodic at 100 Hz, not directly excite that region of the organ?
Can someone explain the workings of the inner ear and detail on why the missing fundamental does not activate the cochlea? Reversely, how can 100 Hz be heard when the cochlea is not even activated at that frequency?

Also tried asking on the DSP community.

I just saw you cross-posted. That's strongly discouraged at SE. I changed the pitch of your question (pun unintended) to make the questions sufficiently different. It's a good question.

The basilar membrane in the inner ear (cochlea) is a place-dependent Fourier transformer (Fig. 1). This means that there is an orderly tonotopic map projected on the basilar membrane (BM). Traveling waves imposed on the BM via the ossicle chain and the oval window start of at the base and travel all the way to the apex. Along the way the resonance frequency of the BM gradually decreases, as the BM gets wider and more flexible (like piano strings).
Now, if a certain frequency is missing, the BM is not moving at that frequency location, and hence the hair cells do not become activated, and the neurons with that specific characteristic are not activated either. How on earth can you still hear that frequency?
It is the harmonic structure that determines our perception of pitch, rather than the lowest harmonic alone. Our brains are sensitive to the frequency difference from one harmonic to the next and base the "real" pitch of the tone on that difference. This is referred to as the "difference tone". When you hear two pure tones, the ear and brain subtract one frequency from the other, and you "hear" a tone with a frequency of this difference (source: National Taiwan University).

Fig. 1. Frequency tuning in the cochlea. source: New York University


text:
Can someone identify the species of this angiosperm?
It seems to be from the pea family (Fabaceae) due to the zygomorphic flowers and the pods. It also has stipules at the base of the composite leaves. It's quite high (~ 80 cm). Photographed in spring in Morocco. It was photographed in a dry riverbed.

This is a difficult one to identify down to the species from the photos. It very much looks like a member of the genus Ononis in the pea family. The leaves, flowers, and seed pods are all characteristic of Ononis. It might be Ononis spinosa, but that is a guess.  The bright sunlight make it difficult to discern many morphological details. I can't see any visible spines on the plant to be certain. Links provided:
https://en.wikipedia.org/wiki/Ononis
https://en.wikipedia.org/wiki/Ononis_spinosa


text:
Can someone identify this species from the pea family?
Can someone identify this species from the pea family? The plant was photographed in Morocco in spring. The location is south of Marrakesh at the foot of the high Atlas, in a dry riverbed.

From Tangier to Agadir passing by Asni in the atlas, you encounter quite a bit of ecological variation in Morocco. It could help to tell where in Morocco and/or what type of ecosystem, you found this plant in (esp. that we can't see the soil from the pictures)!

It would be good in general to have close up views of the flowers and fruits especially in many of these cases, rather than several holistic views.

Also, for Fabs/Legumes, it would be helpful to see a pic of a single compound leaf, picked off and put on a neutral background.

The plant appears to be Medicago arborea. Common names include moon trefoil, shrub medick, alfalfa arborea, and tree medick. It is a member of the pea family Fabiaceae. The species is characterized by the woody stems, the leaves (three), and compressed, coiled seed pods.  See further description in the links below.  It is a native of the Mediterranean basin and apparently becoming rare in nature.
http://botanyphoto.botanicalgarden.ubc.ca/2015/09/medicago-arborea/
https://en.wikipedia.org/wiki/Medicago_arborea


text:
Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective?
Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective? Any answer is helpful. Please let me know.

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

what do you mean by "vaccine statistics" exactly? To me that would denote information about the number of people vaccinated, which would be standard bureaucratic record-keeping. Do you mean statistics on the incidence and/or prevalence of infectious diseases? Or estimates of vaccine efficacy/disease prevention (which would boil down to a comparison of the previous two sets of data)?

Can you please add some more details to your question? Don't simply copy paste the title in the body. Add references, your own research etc to provide background to your question.

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

Not back then.
https://emedicine.medscape.com/article/966220-workup
Although the diagnosis of measles is usually determined from the classic clinical picture (see Clinical), laboratory identification and confirmation of the diagnosis are necessary for the purposes of public health and outbreak control. Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M (IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation.
None of this existed in 1970.

What about Pasteur though? He determined the first vaccine via observation of resistance to symptoms. Don't his observations count as somewhat objective? https://en.wikipedia.org/wiki/Louis_Pasteur#Immunology_and_vaccination

For measles in particular, Koplik's spots, described in 1896, are a fairly reliable diagnostic indicator.

The fact that we have better, more definitive, assays now does not imply that previous assays or clinical observations were purely subjective.


text:
Using formulas to explain why contraction of blood vessels leads to increased blood pressure
I know, I know this is probably a question too simple to be asked on a forum like biology stack exchange. Problem is, I looked many places and can't seem to find a more mathematical approach to explain why the contraction of a BV leads to increased blood pressure (BP).
The main formula i'm looking at is Flow = Pressure/Resistance. In addition, Flow = Area x velocity so Area x velocity = Pressure/Resistance. As the BV constricts, the radius, ie. area, decreases, and so the pressure decreases. But clearly, that is not the case.
What am I missing here?

Basic physiology questions are my personal favourite +1...anyways have you tried it this way (I'm supposing):area decreases, so flow decreases (possibly because resistance (R)  increases in the blood vessel)...now to keep the flow constant the pressure (P) needs to be increased...what I 'm trying to say is that P increases to counter reduced flow as R increases.

There is an important missing assumption in your statement, I've added it in italics:

Contraction of blood vessels leads to increased blood pressure if total flow stays constant.

All you need is your first equation:
Flow = Pressure/Resistance
Decreasing the radius increases the resistance. If flow is constant, then pressure has to increase to get the same flow through the smaller vessel.


text:
How are homing pigeons' "homes" changed?
Last night I was watching the David Attenborough minidocumentary on animal navigation, and it talked about the homing pigeons used in the two World Wars.
Apparently they were donated by UK pigeon fanciers for the war effort.
However, when used as war messengers, obviously they had to "home" back to HQ, not their original UK roost.
How do you "reprogram" the pigeons to use a new home? I assume that pigeon fanciers have to do this all the time if they move house?
(I couldn't find a pigeon SE site so hope this is on-topic here!)

My brother captured a bunch of ordinary pigeons at one building where they had been nesting, then kept them in a second building a couple of miles away for about a month, where they nested and were well fed.  He gave them freedom after that month, and most of them kept coming back to the second building.  I suspect that knowing it was a good home and knowing their flock mates might be found there were factors in their "reprogramming".


text:
Do reproductive organs function before puberty?
Testis means one of the two male reproductive glands that produce spermatozoa and secrete androgens.
Ovary means one of usually two organs that produce oocytes and secrete oestrogen and progesterone.
Do these organs function before puberty?

No, they are not functional before puberty.
For males:

Most males begin puberty between the ages of 9 and 14, but commonly puberty will begin around 12 years old. When the human body reaches a certain weight (which differs among individuals), the hypothalamus releases gonadotropin-releasing hormone. This hormone signals the pituitary gland to release the two hormones that begin the onset of puberty: leutinizing hormone and follicle-stimulating hormone.7 In males, these hormones stimulate activity in the testes, which start to produce the male sex hormone testosterone and begin spermatogenesis. Spermatogenesis is the process of sperm production.

source (warning: contains NSFW drawings and images)


text:
Sex determination in Drosphila
Ive been taught that its based on genic balancing.
But I recently saw this question that has caused me some doubt.
I thought it would be the 1st option but unfortunately they said it to be the 3rd.
But in the answer key, they mention the same line of that of the 1st option.
Ive only been taught genic balance in a general sense .I solved by finding the ratio of no. of X chrom. to no. of autosomes. It would help if someone could give me some clarity.

could you rotate the image or type the question? Hurts my neck to turn it D:

Do not post questions as images. Have the decency to type them out properly so people can read them, especially those who are partially sighted. This is a disgrace.

I think the first possible answer is wrong because maybe by "set" they mean the total number of autosomes. Where as in the figure below it states that the autosome is only responsible for a repressor(Dpn), and that in normal conditions (in pairs i assume) they product equal amounts for females and males.
If the chromosome 2 was not in a proper pair, then I assume the dosage of the Dpn repressor would be off.
The gene dosage is with the activators produced also, sis-a, and sis-b. So I guess in females they produce twice as much activator for the Sxl protein, which later on allows for the repression of male genes and activation of female genes.

There are certain questions that should not be answered. See Not all questions can or should be answered here. The presentation of this makes it fall into that category. Please help to maintain the standards of this site.