text:
Why do we assume that the first humans were dark-skinned?
According to the article Dark skin and blue eyes: How Europeans once looked:

It is widely accepted that Man's oldest common forefather was dark
  skinned, and that people became more pale as they moved further north
  out of Africa into colder climates with less sunlight.

I thought that humans' oldest common ancestor was light-skinned, because

Dark-skinned people have white palms and soles, but light-skinned people have more consistent skin tones. This suggests that light skin is more ancestral and dark skin evolved to protect skin from the sun.
Bonobo chimpanzees, our closest primate cousins, look like they have light skin under black hair.

I understand we all originate in Africa, but I thought that the environmental conditions in Africa were different from today. How do we know that the first humans were dark-skinned?

The first men were not only blacks, they were also homos (If I may)

According to wikipedia, "comparisons between known skin pigmentation genes in chimpanzees and modern Africans show that dark skin evolved along with the loss of body hair about 1.2 million years ago and is the ancestral state of all humans." This is several million years after after the time estimated for the last common human-chimpanzee ancestor, but at least 1 million years before the emergence of Homo Sapiens. This suggests that the earliest species in Homo may have had lighter skin, but that the advantageous genes for dark skin were universal by the time of the first true humans.

The first modern humans evolved about 200.000 years ago in Africa. When they lost their body hair (or at least most of it), they needed some other protection of their skin from the sun - otherwise they are prone to develop melanoma. Melanin is such a protection, and the rate of melanoma is much lower in dark skinned people.
There is also a nice correlation between latitude and skin color - the more to the north (and to some degree to the south as well) you get, the lighter the skin color of the population gets. The reason for this is likely the better ability to synthesize Vitamin D (for which you need sunlight on the skin):

The evolution of human skin coloration.
The evolution of human skin ans skin color.
Development of different human skin colors: a review highlighting
photobiological and photobiophysical aspects.
North-South gradients of melanomas and non-melanomas: A role of
vitamin D?

The lightening of the skin occurred after humans moved to Europe:

The Timing of Pigmentation Lightening in Europeans

And we even know, that this occured more than once, since the genetic reasons for lighter skins are different between europeans and light skinned asians.
A lot of this we know via sequence comparisions of genes involved in pigmentation, there you can trace mutations and see, where they show up first and how they migrate over time. One very good example is the melanocortin-1-receptor (MC1R), which is mutated pretty often in europeans (mutations in this gene are generally associated with lighter skin and hair color; people with red hair carry certain mutations in this gene) but its under selection pressure to not mutate in africa (there are almost no known mutations in MC1R for africans). Another example would be a mutation in the SLC24A5 gene, which is exclusively found in europeans, but not in asians and which accounts also for lighter skin. I stop here for the moment, if there are more specific question, go ahead.

The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model
Genetic Variation at the MC1R Locus and the Time since Loss of Human
Body Hair
SLC24A5, a putative cation exchanger, affects pigmentation in
zebrafish and humans.

Nicely referenced answer.

As per the linked article, new research suggests that Europeans evolved light skin because of diet, not latitude.

+1 for mention of the european 'innovation' of being pale!

@anomal This is discussed, yes.


text:
Where can I get a file/list of the common and scientific names of species?
I am searching for an un-encoded data file with common and scientific names for example of a few hundred species or tens of thousands, where I can search the common and scientific labels of organisms.

English common names or from different countries/languages?

I suggest using Wikidata, although extracting the information may not be straightforward.

English common names would be fine for myself, if you have various related resources it's always good to know.

Uniprot has a list of the controlled vocabulary for common and scientific names of species listed here.
An example entry:
ACAER E  111511: N=Acanthodactylus erythrurus
                 C=Spanish fringe-toed lizard
                 S=Lacerta erythrura

In the example the N is the scientific binomial name (Canthodactylus erythrurus), C is the common name (Spanish fringe-toed lizard).
ACAER is the id code, 111511 is the code for the taxonomic node, E means it is a eukaryote, and S is a synonym of either name.

The list contains 25336 scientific names currently, which falls short of the ~2.5m species in GBIF, or the 10s, or 100s of millions that are estimated to exist. The Uniprot list does, however, represent every organism included in Uniprot, which is widely regarded as being among the most comprehensive protein databases that exist today.

That's a fairy short species list though, if it is meant for general-purpose use (i.e. not specifically in relation to Uniprot data).

This is a worthwhile point. Uniprot hold additional lists for different strains that may account for some of the difference (i.e GBIF count each strain as a separate name, Uniprot packs many strains under 1 species name-not negligible for bacteria). I cannot verify any redundancy measures taken by GBIF and I cannot find any peer reviewed article of GBIF. This would explain a lot of over-estimation since both Uniprot and GBIF are pulling species names from many of the same external databases.

Just a note here, this list includes many viral strains, which may or may not be something you want.

Maybe not a direct answer to your question, depending on what you mean with "unencoded data file", but the Global Biodiversity Information Facility (GBIF) has an API where you extract data for species names. Their database includes common names (aka vernacular names) when they have that, and often common names from different languages. Using this API, you can extract data and construct a name file for a particular taxa that you are interested in.
As an example, this is the list of the first 20 vernacular names found for Passer domesticus (House sparrow):
{
   "endOfRecords" : false,
   "results" : [
      {
         "language" : "",
         "sourceTaxonKey" : 100220560,
         "source" : "Global Invasive Species Database",
         "vernacularName" : "English sparrow"
      },
      {
         "language" : "",
         "sourceTaxonKey" : 100220560,
         "vernacularName" : "Europese huismuis",
         "source" : "Global Invasive Species Database"
      },
      {
         "vernacularName" : "Gorrion domestico",
         "source" : "Global Invasive Species Database",
         "language" : "",
         "sourceTaxonKey" : 100220560
      },
      {
         "source" : "Integrated Taxonomic Information System (ITIS)",
         "vernacularName" : "GorriÃ³n casero",
         "language" : "spa",
         "sourceTaxonKey" : 102101640
      },
      {
         "vernacularName" : "Gorrión Común",
         "sourceTaxonKey" : 123213203,
         "language" : "spa"
      },
      {
         "language" : "spa",
         "sourceTaxonKey" : 101186844,
         "source" : "The European Nature Information System (EUNIS)",
         "vernacularName" : "Gorrión Común"
      },
      {
         "language" : "spa",
         "sourceTaxonKey" : 114130266,
         "source" : "Colaboraciones Americanas Sobre Aves",
         "vernacularName" : "Gorrión casero"
      },
      {
         "vernacularName" : "Gorrión casero",
         "source" : "Yanayacu Natural History Research Group",
         "sourceTaxonKey" : 119245200,
         "language" : "spa"
      },
      {
         "vernacularName" : "Gorrión casero",
         "source" : "Catalogue of Life",
         "sourceTaxonKey" : 119950016,
         "language" : "spa"
      },
      {
         "language" : "swe",
         "sourceTaxonKey" : 101186844,
         "vernacularName" : "Gråsparv",
         "source" : "The European Nature Information System (EUNIS)"
      },
      {
         "vernacularName" : "Gråspurv",
         "language" : "dan",
         "sourceTaxonKey" : 123213203
      },
      {
         "vernacularName" : "Gråspurv",
         "language" : "nob",
         "sourceTaxonKey" : 123213203
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 116795880,
         "vernacularName" : "Haussperling",
         "source" : "Taxon list of animals with German names (worldwide) compiled at the SMNS",
         "country" : "DE"
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 100483595,
         "source" : "Belgian Species List",
         "country" : "BE",
         "vernacularName" : "Haussperling"
      },
      {
         "language" : "deu",
         "sourceTaxonKey" : 123213203,
         "vernacularName" : "Haussperling"
      },
      {
         "sourceTaxonKey" : 101186844,
         "language" : "deu",
         "source" : "The European Nature Information System (EUNIS)",
         "vernacularName" : "Haussperling"
      },
      {
         "source" : "The Clements Checklist",
         "vernacularName" : "House Sparrow",
         "language" : "eng",
         "sourceTaxonKey" : 113987294
      },
      {
         "vernacularName" : "House Sparrow",
         "source" : "Taxonomy in Flux Checklist",
         "language" : "eng",
         "sourceTaxonKey" : 100159046
      },
      {
         "source" : "Colaboraciones Americanas Sobre Aves",
         "vernacularName" : "House Sparrow",
         "language" : "eng",
         "sourceTaxonKey" : 114130266
      },
      {
         "sourceTaxonKey" : 102101640,
         "language" : "eng",
         "vernacularName" : "House Sparrow",
         "source" : "Integrated Taxonomic Information System (ITIS)"
      }
   ],
   "limit" : 20,
   "offset" : 0
}

Using this type of search: api.gbif.org/v1/species?name=Passer%20domesticus, you can look for all info for a particular species, starting from either a scientific name or a common name (in example, Passer domesticus).
GBIF includes information in 1,643,948 species (and counting), but I don't know for what proportion they have common names (or where there are common names).

species names in many languages. Awesome thankyou.

They seem to have some Unicode encoding issues, though. Not only does the API not specifically indicate via HTTP headers that the text it's returning is UTF-8 encoded, but some of the vernacular names (like "GorriÃ³n casero" above) actually appear to have UTF-8 encoding applied twice.

@IlmariKaronen True. And thanks for the reformatting.

A lot of this data is also downloadable from GBIF: for example, if the Global Invasive Species Database seems to have the names you want, you can search for it at http://www.gbif.org/dataset -- many (most? all?) of the datasets can be downloaded as a "Darwin Core Archive" (a ZIP file containing CSV files) from the dataset page (http://www.gbif.org/dataset/b351a324-77c4-41c9-a909-f30f77268bc4).

If you're looking for marine species, the World Register of Marine Species is probably the best place to find this information.
The Ocean Biogeographic Information System also contains a tremendous amount of marine species.

Thanks alot. I was looking at flying fish today, the Uniprot list has at least 11 flying squid and flyingfish. thanks for the resource.

A late answer, but I think the mentioned sources are limited and the awesome download page of Observado.org offers a much better alternative.
The  website of Observado, an initiative to collect species observations worldwide, has global species lists in csv format that are as complete as possible. The plant list currently has 381.473 records! You can download local species names in more languages you might have heard from, from English to Russian and from Frysk to Dzongkha.
Note that these lists are meant for observations in the field, and hence also contain multispecies, hybrids and synonyms. But these can be filtered out easily.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What are the advantages and disadvantages of being ambidextrous?
Most of us have one dominant hand. We find it nigh on impossible to do very delicate or dextrous activities with our other-hand. This seems like an apparent weakness, and a rather odd one when you first think about it.
Cursory internet searches revealed unexpected findings. One website said it has mostly negative effects on the brain. However I don't trust the source at all.
I'd be interested to know about the "story" about the good and bad of ambidextrous physiology. Particularly, I am interested in the neuroscience of ambidextrous people.

It would also be interesting to know whether our ancestors used both the hands and using just one hand is  recently evolved

@biogirl great comment needs more attention from everyone

@agha rehan abbas Thanks ! Thinking about something from evolution point of view always helps.

@biogirl It's a contentious issue, but chimps do indeed display handed-ness for tasks like termite fishing.

I think that the advantages of using both hands with equal ease is quite evident whether it be sports, at your work or while you are doing your household chores.

An obvious advantage is using both hands to write or draw with both at the same time.
I would be focusing on the disadvantages that may be faced.

1) Ambidextrous people are more prone to suffer from Synaesthesia
  (reference)
2) They are likely to possess (not necessarily) the LRRTM1 gene which
  is linked with Schizophrenia (reference).
3) They score lesser in intelligence testing (reference).
4) Mixed handed children are more likely to suffer from ADHD
  (reference).
5) Mixed handedness is associated with greater age-related decline
  (reference)
6) They are easier to anger and influence emotionally (reference).

There are quite a few studies that have pointed out that it may not be all that good a condition but Leonardo da Vinci who was probably the most diversely talented man who ever lived is said to have been ambidextrous. He apparently could draw with one hand and write with the other at the same time, so I would have to say that the positives of the condition are extremely good (reference).
edit:
This probably qualifies as a second question :-D but I just saw a thought by biogirl in the comments section on "whether our ancestors used both the hands and using just one hand is recently evolved" and she has a point there. From a study publlished in 1977 I quote.

The predominance of the right hand over the left was also reported
  among Egyptian art forms 3,500 to 4,500 years old, where the ratio of
  left- to right-handers was 9:111 and 5:100, respectively. However,
  going further back using the "Draw-a-Man Test," found that ancient
  paleolithic man, from 1,750,000 to 8,000 years B.C., was probably
  either more ambidextrous or that there was a greater proportion of
  left-handers than there are now. (reference)

Also from a study titled "Evolutionary Back Grounds of Human Left Handedness", the authors concluded that

For most manual tasks, especially those tasks involved in competitive
  activities, increasing performance by the specialization of one hand
  is certainly adaptive. Aggressive interactions are responsible for
  fundamental selection pressures acting during primate and human
  evolution. The higher prevalence of right-handedness might well be due
  to a previously existing cerebral bias. But the specialization of one
  forelimb leading to right or left-handedness is better viewed as the
  result of natural selection. (reference)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How early can we know the sex of a human being now?
Do we need to wait till a Zygote forms?

Quite early when combined with IVF.
At present there are two method that are available for use.
The first is genetic testing of preimplantation genetic screening (PGS). A single cell is taken from the embryo and tested for sex by genetic testing. Only the right sex embryo is implanted. http://www.babycenter.com/0_choosing-your-babys-sex-what-the-scientists-say_2915.bc?page=1
The second method is the Ericsson method, which is based on the fact that Y sperm swim faster than X sperm, as the Y sperm are smaller.
http://www.babycenter.com/0_choosing-your-babys-sex-what-the-scientists-say_2915.bc?page=2
At present there is also a 3rd method that is used in animals but has not gain FDA approval for human use. And that is sperm sorting using florescence activated cell sorting (FACS). In this method a flow cyctometer is used in conjunction with a non-toxic cell permeable DNA dye. the idea here is to sort sperm based on their DNA content. X sperm have more DNA than Y sperm as the X chromosome is bigger than the Y chromosome. This method is called Microsort https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256056/. Primary concerns is that the DNA might cause DNA damage.
An older method that was greatly used between 1970 to early 1980s to sort sperm by sex was density gradient centrifugation. The idea being X sperm being denser than Y sperm as the X chromosome is bigger than the Y. This method of gender sorting is still available in some IVF clinics but medical studies indicate that the method is ineffective http://www.ingender.com/gender-selection/ericsson/Percoll.aspx
More stuff to read about
http://www.reproduction-online.org/content/145/1/R15.full
http://chooseagender.com/methods-of-gender-selection.aspx.

Can you please provide a source showing that X and Y sperm can be separated via centrifuge?

The link to IVF lab in my answer states that they use centrifugation to separate X and Y sperm. Even success rate and the cost that they will charge. However if you want a scientific paper, here is one. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169681/ Or wikipedia if preferred https://en.wikipedia.org/wiki/Sperm_sorting

The Wikipedia article is about general sorting. The paragraph about centrifugation is for sorting by sperm quality, not X/Y. Flow cytometry is the one that can be used for differentiation, stating "...flow cytometry is the only currently used technique able to determine the sex of future progeny...". The second article is interesting, but I'm not sure if it actually indicates that the centrifugation is what's actually used for sorting sperm, rather than mixing and separating out additives, and it seems to indicate that the methods aren't very successful. Someone else should weigh in on that.

Hmm.. while centrifugation of sperm to separate out X and Y sperm has been done for the last 30 years, it appears that the method has fallen out of favor. I will change the answer to reflect this and thrown in more stuff I have read about on this subject.

@Jay  I mean for a normally combined XX or YY,  how do know it is XX or YY after they combine. It is different with we can control which combines with Y.

Oh. It depends on how daring you are. Using amniocentesis you can sample the amniotic fluid and obtain cells. And test those cells. Amniocentesis is typically done at 16 wk http://www.webmd.com/baby/amniocentesis-17766 But some facilities will do it as early as 11wk http://americanpregnancy.org/prenatal-testing/amniocentesis/ But the earlier you do this, the higher the risk of a spontaneous abortion. If you use ultrasound to tell the sex of the fetus, it is 16-20wk http://www.babycenter.com/404_when-and-how-can-i-find-out-my-babys-sex_10366575.bc?PageSpeed=noscript

Before the zygote, there is no individual for which sex can be defined! However, it is possible to know the sex of the future zygote if you know the gametes that are going to fuse.
In humans, just like in all placental mammals (which excl. kangaroos and platypus), sex is defined by sexual chromosomes, where males are XY while females are XX. A mother can therefore only pass on an X (and have no influence on the sex of the offspring) while a father can pass on either an X or a Y which will determine the sex of the offspring. Knowing the paternal gamete (the spermatozoid), one can infer what the sex of the future offspring will be. Of course, in one ejaculate, there are about as many X-bearing gametes than Y-bearing gametes.
Technically speaking, could typically make a karyotype to infer whether chromosome X or Y is being transmitted.

@SanjuktaGhosh Remi said "possible to know the sex", not "know the possible sex" i.e. if you know what sex chromosome the sperm is carrying, you can tell what zygote will result.

@Remi How to know that technically for a normally combined XX or XY?

Make a karyotype (info edited in the post). Does this answer your question?

@Remi  If we do not consider ethics, once a X-Y or a X-X combine, we can find it and do karyotype?

Do you mean "fuse" (like after fecundation) by saying "combine"? What is "it" in can we find it? You can do a karyotype on any cell (whether haploid or diploid). On diploid human cells you can infer sex from karyotype. On haploid human cell, the concept of sex makes no sense but you can still infer whether the haploid cell carries an X or a Y chromosome

So after the combination of an egg and a sperm, before sex organs develop (7-12weeks), it is still possible to infer sex, right? Have human beings proved a particular egg does not tend to select an x sperm or a y sperm? (I know apparently it is in a passive mode.)

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


text:
Determine percentage of crow hybrids
We had in class following question which I had no idea how to get to the correct answer:

The carrion crow and the hooded crow are fertile together,  but their
  reproductive success is reduced by 50%. In a certain region exist
  two populations of both species of roughly the same size. Thus,
  mixed couples occur in about 10% of all cases. What is the percentage of
  hybrids in the F1-generation?

(Translated from German.)
I thought it would be something like 5/95 = 5,3% but apparently the answer is 1%. Why?

why do you think it would be 5/95? and how, according to you, can the answer be 1%? please show some research effort before asking question here.

1% is the answer according to the solution. 5/95 because 90% of the couples have 100% success, and 10% have 50% sucess.  @another'Homosapien'

Homework questions are off-topic here unless you show some research effort. Tell us what research effort you have put on the question, lest this question is likely to be closed.

Well I told you what I thought was the correct approach. I did not find any hints in our material. I did further research before posting here. I didnt find any source dealing with mathematical discussions of this topic. Further, to me my solution seems correct. @another'Homosapien'

In order to make your reasoning clearer, you should use more formal notations and explain your thinking step by step. Here's a proposition.
Let's use the following notations :

$C$: the total number of couples (mixed and not mixed)
$r$: the reproductive success
$F1_h$: the number of hybrids in the F1 generation
$F1_{nh}$: the number of non hybrids in the F1 generation

You are looking for the percentage of hydrids in the F1 generation, which is:
$x = \frac{F1_h}{F1_h + F1_{nh}}$
You know that $10~\%$ of the couples are mixed couples and that their reproductive success is reduced by $50~\%$. This can be written:
$\begin{cases} 0.9\cdot C \cdot r = F1_{nh} \\ 0.1\cdot C\cdot \frac{r}{2} = F1_h \end{cases}$
Thus: $\displaystyle x = \frac{F1_h}{F1_h + F1_{nh}} = \frac{0.05\cdot C\cdot r}{C\cdot r\cdot 0.95} = \frac{0.05}{0.95}$
This is indeed the result you suggested. So the correction you were given might not be correct. Or maybe there was some more information in your homework that you ignored...


text:
What is the formula to establish ec50 reproducibility with respect to dose response curves for some drug?
The EC50 is determined by fitting a standard curve to the experimentally obtained control values for each dose response curve using some software that does trial and comparison until satisfactory(nonlinear regression).
In the literature, it is mentioned that experimentally obtained control values for the dose response curves, are EC50 reproducible. To my current understanding meaning that EC50's obtained for different for several dose response curves are actually 'close enough'(in some formal statistical sense) together. Is there some procedure or formula for formally establishing EC50 reproducibility?
Thank you :)

Welcome to Biology SE. What do you mean by "trial and error"? EC50 analysis is usually done by nonlinear regression, typically with some sigmoid function. There are many methods for estimating variances / confidence intervals for parameters in nonlinear regression, so if you can give a bit more details about your specific model and data, that might help. Also, the Statistics SE might be appropriate for your question.

Hi Roland, thanks for your reply! Actually from your reply I can phrase better what I meant to ask. Basically a sigmoid is fitted to experimental data using nonlinear regression as you said for each experiment. Now the aim is to  conclude reproducibility of these sigmoids for added experiments(dose response curves). So basically comparing the fit parameters(EC50, slope) and establishing that they follow a concentrated pattern. Some researchers refer in articles to this as 'EC50 reproducibility'. I was wondering whether there are widely used methods of establishing this reproducibility.

And the data itself is confidential btw. But the model used is basically a sigmoid as you mentioned. Thank you for your reply.

If you have multiple EC50 estimates from separate independent measurement series, then it should be easy to see if they are in agreement?  You could do mean +/- std dev of the EC59 values (assuming a normal distribution), but personally I prefer just tabulating/plotting the data.  If the data is tight, is usually obvious.  The situation is more tricky when there is only one measurement series and some variances estimate must be derived from the regression analysis.

The DRC package, in the paper from my answer, includes functions to directly compare parameters such as the slope, from nonlinear regressions.

Thank you for your reply Michael_A. I'm looking at the article.

The different models that can be used to fit the curves do differ.  The linked paper and this website outline the differences; the discussion revolves around an R package called DRC but much of the information is generally applicable. Modelling can also be used to estimate ED50.
The parameters and models that are being used need to be consistent with the biology that is being studied. If it's appropriate, scaling the upper and lower bounds of your data can improve the consistency of ED50 estimates as this removes the requirement for the model to estimate those parameters. Something like this can be used for scaling;
(VALUE - topdrugmean)/(nodrugmean-topdrugmean)

The Akaike Information criterion can be used to measure the goodness-of-fit for different models (see the preceding links).


text:
What bird is this?

Location: Urban area near the Western Ghats, Kerala, South India.
Date: 20th April, 2017
Current Climate: Hot and humid. Occasional rains.
Brief Description:
Not large, about the size of a house sparrow. Didn't make any characteristic sound/chirping during the period of observation. Pointed,slightly curved, thin beak. Probably feeds on insects, grain, nuts. Has a black crest atop its head, similar to that of a woodpecker. Appears to have an off-white or pale yellow "mouth" (couldn't get a picture of that, sorry). Chin and throat have white feathers. Foot and legs appear dark gray, if not black. Possesses conspicuous red infraorbital patches (of feathers?) below each eye.
Additional Information:
The locality is often frequented by feral pigeons. However, this particular bird made its appearance when there were no pigeons in sight.

That is a red whiskered bulbul.

(image from the Wikipedia article)
The crest isn't as prominent in your pictures - maybe it has just been to the barbers.


text:
Glycolysis - ATP production
In glycolysis, 2 ATP molecules are produced from each triose phosphate molecule (to give a total of 4 ATP produced; 2 net produced as 2 were initially used up in the reaction).
I don't understand how this would be the case, as each triose phosphate only has one phosphate group available to form ATP from ADP, meaning that one ATP is produced per triose phosphate. I know this cannot be the case as this would mean a 0 net production of ATP defeating the purpose of glycolysis, but i can't get my head around why.
out of curiosity, would the other remaining two phosphates that are required come from other sources, i.e. 2 phosphates + the 2 phosphates already from the two trios phosphate molecules to give us the 4 ATP molecules (2 net ATP)
Many thanks in advance.

Possible duplicate of Where do the four ADPs come from in the second stage of glycolysis?

@VanceLAlbaugh — I agree that the two questions are related and would be better as one, but the other question wants to know where the ADPs that accept the phosphate come from, whereas this asks about where the phosphates that are not from ATP come from. That is not covered in the other question or its accepted answer.

Though David has already answered as I wished to write one for this question here's my answer$-$
You say that

In glycolysis, 2 ATP molecules are produced from each triose phosphate molecule ... I don't understand how this would be the case, as each triose phosphate only has one phosphate group

but you are wrong here as each triose phosphate is destined to undergo phosphorylation before they are dephosphorylated to yield 2 ATPs each.
Here are the reactions:
You can see that out of the two trioses Glyceraldehyde-3-phosphate is phosphorylated into a compound (1,3-bisphosphoglycerate) that has two phosphoryl groups. Similarly Dihydroxy acetone phosphate the other triose is first converted into glyceraldehyde-3-phosphate by an isomerisation reaction catalysed by triosephosphate isomerase. This glyceraldehyde-3-PO$_4$ formed undergoes phosphorylation to form a two phosphoryl group containing compound.

would the other remaining two phosphates that are required come from other sources..?

Yes the Phosphate group added to Glyceraldehyde-3-PO$_4$ is derived from orthophosphate (HPO43−).

Probably just loose writing. I imagine what the OP meant was something like "In the second stage of glycolysis, after one hexose is converted to two triose molecules in the aldolase reaction, each of these produce 2 ATPs". And his concern seemed to be that the aldolase reaction produced  triose monophosphates (from the previous di-phosphorylated hexose) so where did the other phosphate come from? He was looking for more ATP input and failed to notice the orthophosphate.

@David Probably.

@David I have seen people using the term OP quite often here. What does it stand for? Is it Owner of Post?

— I believe it stands for Original Poster, but don't quote me on that. Certainly it refers to the person who posted the question. I really shouldn't use it because Poster takes no time to write, and acronyms like this present a barrier to new users. They imply that there is an in-group who know these things. That is why I have always kicked students hard who write dissertations full of lab abbreviations. After that I guess I'll have to refer to the poster in future.

@A.P Does this answer clear your doubts? Let me know if I could help.

The other two phosphates come from inorganic phosphate* in solution (Pi — in my diagram below) at the glyceraldehyde phosphate dehydrogenase stage. (Two, of course, because there are two molecules of triose.)

This is covered in Berg et al. Section 16.1.5.
*The term inorganic phosphate is used because there are various different anions in solution derived from phosphoric acid, depending on the pH. At physiological pH the predominant species is the double-negativly charged, monohydrogen phosphate.


text:
Calculating the ripeness rate in fruits
I need a way to calculate avocado ripeness rate in my experiment so I need a quantitative way, I'm not sure if calculating the cellular respiration for the avocado will result in ripeness rate for the fruit, if that's true I need references if you got.
And if you got another better quantitative ways to get the "rate" of the fruit ripeness.

Generally, ethylene production is used to gauge fruit ripeness.  This paper (PDF download) outlines an experiment measuring ethylene production from Hass avocados at different temperatures over several days.  It appears they used gas chromatography to measure both ethylene and CO2 concentrations.

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


text:
Insect Identification Request - Is this a Satin Moth or something else?
Date:     July 2, 2018
Time:     11:00 AM
Location: Minneapolis MN
Size:     Approx. 1" from head to tail

I saw this moth at work today. I wasn't sure if it was just a Satin Moth, an albino (it seems to have some pigment), or something else. It fluttered over to the door and landed there to rest. A few minutes later it disappeared.
I would really appreciate some help identifying it. Please comment if I need to add additional information.


text:
What is the benefit of oxygen tanks to persons trappped in an enclosed space?
When people are enclosed in an air-tight space, the levels of carbon dioxide will rise to lethal levels (hypercapnia) long before the oxygen is exhausted (hypoxia).  For example, the astronauts of Apollo 13 were in danger because the carbon dioxide scrubbers in the lunar module were inadequate.  They never "ran out of oxygen", even though the oxygen tank of their service module exploded.
What would be the benefit to supplying such persons with tanks of additional oxygen?  It seems to be a futile gesture to me.
The reason I ask is a news story ongoing for several weeks.  Twelve children and one adult have been trapped by water in a cave for several weeks.  At the time this question was written, four boys were already rescued.  Officials have repeatedly expressed concerns that the "oxygen is running out" and are placing oxygen tanks in the cave.  Is there any benefit to this, or are officials simply ignorant of human physiology?

By breathing oxygen from a tank you can reduce hypercapnia. As Astrolamb below also indicates; O2 eliminates CO2 from the body; it's a balance

The quantity of CO2 is less important than concentration. By increasing the quantities of O2, you decrease the concentration of CO2, thus reducing hypercapnia.

@AliceD: That's a great solution, until your tank runs out.  Then you are back to breathing the ambient air, which now has even more CO2 than you started with!

@DrSheldon, alas yet obviously, nothing in existence today lasts eternally

@Astrolamb: Increasing the amount of O2 (or other gases) would hypothetically work, but wouldn't it be far more efficient (e.g. doubling the ambient air volume to halve the pCO2) and practical to use a CO2 scrubber?

CO2 scrubbers are very costly compared to the relative ease by which oxygen is generated. Additionally, they are far more efficient when scrubbing high concentrations of CO2, such as exhaust gases, than the lower concentrations of ambient CO2.

The big issue in the case of the cave is that it is a temporary thing. O2 only needs to be supplied until the trapped people are rescued, and scrubbers are too expensive relative to O2 costs to be used for such a temporary situation. This is hugely different from, say, the ISS, which is intended for long-term occupation. For the ISS, using scrubbers is much more practical.

@Astrolamb, good answer - you might as well compile your comments into a full-blown answer, makes perfect sense. Just add a few web links here and there and it would receive my upvote for sure.

I'd add that we don't know the dimensions, ventilation conditions, altitude, and other important aspects of the chamber in this case. A cave is a very different environment from a lunar module. It is certainly not air tight.

"...or are officials simply ignorant of human physiology?" You assume much.

@Astrolamb: The cost aspect is good point.  Also, oxygen tanks are more likely to be on-hand than CO2 scrubbers.  However, neither of these have to do with the "running out of oxygen" claims of the press.  Then again, during Apollo 13 the press incorrectly first reported the astronauts "running out of oxygen."

I'm confused - how does having more oxygen tanks NOT have something to do with running out of oxygen?

@Astrolamb: Do we genuinely know if the oxygen is running out?  We have press reports, but the press has been wrong before, as it was in Apollo 13.  We can't assume that the O2 concentration has actually been measured.  I have yet to read an actual value of O2 concentration, nor have scientific terms such as "hypoxia" been used.

I think that to the uninformed public, high CO2 concentrations is effectively equivalent to "running out of oxygen", so comments from the press are moot. I'm sure the officials have consulted people who actually know what they're talking about.

I don't believe they are supplying oxygen tanks to reoxygenate the cave...they are supplying oxygen tanks to be able to ferry people over 1 km underwater. They feel pressure to do this quickly because oxygen levels are dropping and presumably CO2 levels are rising in the small space the individuals are in. Separate issues, likely confused in news.

@BryanKrause that's what I thought too (the oxygen was for diving, not for the boys while they're sitting in the cave), but in this cbc report it sounds like they actually ran an $O_2$ line into the cave.

@DanHall Thanks for that source, I had looked briefly and didn't find ; I also had thought of natural CO2 sequestering in a cave system and I think your answer covers that well. I wonder, too, if by "oxygen line" they really just mean "compressed air" as in a typical mine ventilation system.

@BryanKrause I wouldn't be surprised if they did (mean compressed air rather than oxygen)

"They never "ran out of oxygen", even though the oxygen tank of their service module exploded." The oxygen tanks in the service module exploded, but they still had the oxygen tanks in the lunar module, which provided sufficient oxygen for the "quick return" flight path back to earth. It wasn't like they survived four days on the ambient oxygen in the cabin at the time of the accident. To sustain life you have to have both a supply of oxygen and a way of limiting $CO_2$ concentration.

There are a couple of ways to answer your question. If we assume the cave is an air-tight chamber, we've entered the domain of a very specialized field in medicine, so I can't speak as authoritatively as I'd like there, but lets start, with the fact that the cave is not air tight.
It's a cave
A cave is not a submarine or a lunar module. It is not air-tight, but in a large environment with various types of gas exchange. The cave may already have it's own $CO_2$ scrubber of a sort, since common minerals reversibly bind $CO_2$. I expect there is a whole science around $CO_2$ cycles in, e.g., limestone caves, but the point here is there is likely a sink of some sort for the $CO_2$ produced by the boys. For example, I think we could reasonably speculate that the following equilibrium in a limestone cave would be driven to the right with additional $CO_2$:
$CaCO_3 + H_2O + CO_2 \rightleftharpoons Ca(HCO_3)_2$
Why would you give oxygen?
Here I can speak authoritatively. I'd refer you to both of West's excellent texts (Respiratory Physiology and Pulmonary Pathophysiology) for further reference.
Lets clear up a misconception in the comments. It is correct that we're concerned about the concentration (typically expressed as partial pressure) of gas, not the amount. It is not correct that $O_2$ eliminates $CO_2$ from the body. This can be confusing, but it is a misapplication of Dalton's law to human physiology, based on a misunderstanding about where and how the gas is exchanged. By Dalton's law, you can reduce the concentration of $CO_2$ in a container by increasing the concentration of some other gas (e.g., $O_2$). If $CO_2$ is accumulating in the cave (rather than being taken up by the environment), then delivering compressed gas with no $CO_2$ would decrease the concentration of $CO_2$ in inspired air. Inspired air, however, is not the same as alveolar air or arterial or venous gas, and the human body is not well modeled as a container full of various gases.
While it is true that when $CO_2$ is retained in respiratory acidosis, arterial $P_{O2}$ must go down by whatever amount arterial $P_{CO2}$ goes up, it doesn't work the other way around. Delivering a higher $F_{iO2}$, or fraction of inspired $O_2$ does not cause an inverse change in arterial $CO_2$. This ends up being fairly complicated, and a full discussion is beyond the scope of this question. Let me just emphasize that supplemental $O_2$ specifically treats low $O_2$ (or, in a very specific case, $CO$, carbonmonoxide, poisoning). High $CO_2$ is treated by increasing ventilation. In fact, there are a few special cases where supplemental $O_2$ actually increases a patient's $CO_2$ levels, two of which involve hypercapnic respiratory failure. We do give $O_2$ for hypercapnic respiratory failure, but it is given to treat the associated hypoxia, not the hypercapnea. The only way to decrease $CO_2$ is to increase ventilation. This is a very important concept in critical care and respiratory medicine. I'd refer you to West Pulmonary Pathophysiology, Chapter 10, or any critical care textbook.
So, back to the reason you might want to give oxygen...
CNN reports that oxygen levels in the cave have reached 15%. If the atmospheric pressure of the cave is 760mm Hg, then the $P_{O2}$ in inspired air is about 107mm Hg, ((760 - 47 for water vapor) * 0.15, see West Respiratory Physiology, or any physiology text). At 600mm Hg (equivalent to an elevation of ~2000 meters) $P_{O2}$ in inspired air is 83mm Hg. This is low, and could start to be a problem (leading to hypoxemia and hypoxia), depending on the ability of the boys to compensate (again, see West, either respiratory physiology or pulmonary pathophysiology). If the $O_2$ levels in the cave continued to drop, or if the boys weren't compensating well, then it would be reasonable to give supplemental oxygen to treat their hypoxia, regardless of what the $CO_2$ levels were.
But if $O_2$ was low, wouldn't they also have to have high $CO_2$?
I'm not an expert in cave ecology, but it doesn't seem that strange to me that the rate of $O_2$ consumption by the boys could exceed the environment's capacity to produce or release $O_2$ from organic sources, dissolved sources, or ventilation, without their rate of $CO_2$ production overwhelming the environment's $CO_2$ sink. I have no good evidence one way or the other for this speculation.
What if it is an air-tight container?
Atmospheric $CO_2$ is on the order of 400ppm, or 0.04%. Normal levels in the body are 5% (40mm Hg / 760). We rely on this gradient to dump the $CO_2$ produced by cellular respiration using ventilation, but can still operate, with difficulty, with 5% $F_{iCO2}$. Serious problems (same reference) occur at higher levels. Again, in this particular case we're beyond my personal expertise (Dammit, Jim, I'm a doctor, not an aerospace or submarine doctor!), but in an air-tight container without a $CO_2$ sink, if $CO_2$ levels were higher than 5% and rising, I'd expect you would need to directly address $CO_2$. If it's a small container, adding other gases from pressurized canisters, or pumping gases in would decrease the $F_{iCO2}$ by Dalton's law, provided you could overcome the rate of $CO_2$ production by the boys. If $CO_2$ had accumulated in the boys blood (hypercapnea), they would (need to) increase their ventilation as well, adding more $CO_2$ to the chamber.


text:
Appropriateness of PCA to visualize clusters in genetic data
In many genetic studies, PCA is often utilized to examine genetic cluster in human populations. Rarely is the % variance reported for the components. With human data it's been my experience that the first three components (which are often plotted) tend to contain very little % of the variance. How meaningful are your visual results (i.e. clustering) when the first three components cumulatively account for only (say) 10% of the variance?
To answer this question, I constructed a theory based on the following assumptions.
One theory. For human, the proportion of variation within groups (i.e. same ethnic group) account for ~85% of the genetic variation within individuals. Conversely, the variation within populations (i.e. continental scale) account for only ~15% of the genetic variation within individuals.
Even though the first three components (i.e. PC1, PC2, PC3) contained only a small fraction of the total variance, most often the magnitude of associated eigenvalues can be 50 to 70 times that of higher components. In other words, the first three components can explain substantially more (50x-70x) variance than any other component when comparing by individual basis.
While sometimes these higher components do explain hidden substructure within groups, bear in mind that individuals from the same group has ~85% genetic variation among themselves. Hence, most of the higher components might just be explaining this within groups variation. For analysis of genetic clusters, this is of no interest to geneticists. These higher components can thus be treated as background noises. Geneticists are mainly interested in variation within populations, which often is very ancient and strongly separated. Thus, when population clusters are formed in the first three components, it can be argued that they form mainly due to the variation within populations.
Summary: The low variance (<10%) cumulatively accounted by the first three components can be justified by the fact that variation within populations is only ~15% of the genetic variation within individuals.
My question is: Does the theory to my own question seem reasonable?

I'm sure you agree this is a question about statistics, not biology. Geneticists use statistics, but many of us are not experts and often require recurring reminders from statisticians on how best to interpret, analyze and visualize data, preserving both clarity and validity. I agree; the principal components should always account for as large amount of variation in the data as possible, otherwise it would make little sense - at least in my limited understanding of it. I defer to others on this question!


text:
Why is the manchineel tree so poisonous?
The machineel tree is incredibly toxic to humans. What advantage could Hippomane mancinella have for being so poisonous? It's name even apparently translates to “little apple that makes horses mad”.
Is it an incidental toxin, or an evolutionary hangover from a previous predator, or is it still actively predated by a species with high immunity?
I ask because this seems somewhat paradoxical; the tree has fruit, yet is toxic to animals.

I found an answer at http://www.atlasobscura.com/articles/whatever-you-do-do-not-eat-touch-or-even-inhale-the-air-around-the-manchineel-tree.

I answered a catch-all version of this: http://biology.stackexchange.com/questions/36977/how-did-zootoxins-evolve/36979#36979 The same applies to trees.

I've made some drastic edits to the post to make it answerable (it was a bit rambly)! Feel free to roll back; I may have changed the question in some way unwittingly. Also, your linked article doesn't answer the question you asked. It unverifiably says iguanas have been seen eating it in one continent, and that nobody knows why it's toxic to humans.

The sap is full of Phorbols. Phorbol esters are so carcinogenic, labs use them to cause cancer in animal models.

@James The question you linked is asking about animal venom, which may not be completely relevant to this question.

@MarchHo I can't image plants would be exempt. They absolutely could get stuck in an arms race in order to not to be predated upon. Perhaps iguanas which don't seem to be affected are eating the seeds which should be dispersed by the fruit decaying. The plants that are more toxic become more prolific at dispersal et cetera. Of course, my argument is moot without a bona fide example! I never meant to imply this is a duplicate question, but an answer may touch on similar elements.

The article I linked gives a theory about the evolutionary reason that probably wasn't proven but doesn't give a biological reason.

According to http://www.atlasobscura.com/articles/whatever-you-do-do-not-eat-touch-or-even-inhale-the-air-around-the-manchineel-tree, it evolved to be poisonous to discourage animals from digging into it. Here's one possible way that could have happened. It was once only a tiny speck more poisonous than other trees by random fluctuations in toxicity. By natural selection, animals evolved to prefer it less. They were more likely to dislike the taste of the more poisonous manchineel trees, which in turn caused it to evolve to be more poisonous. Maybe it was such an advantage to get more energy by eating some of it that some species evolved to be more resistant to the poison so that they could eat some of it. That caused the manchineel tree to evolve to be even more poisonous to discourage animals from eating it. It was an evolutionary disadvantage for the apples to be poisonous. That was just an accidental result of the rest of the tree being so poisonous. Indeed, they did evolve to be much less poisonous than the sap for that reason. Animals evolved to dislike the taste of the apples because they're poisonous. The less poisonous ones were more likely to get eaten and have their seeds spread. Since they couldn't evolve to be nonpoisonous, they instead evolved to taste like there's nothing wrong with them so that they could get eaten. Since iguanas did evolve to be immune to the poison apples, there wasn't much of an advantage in them evolving to be even less poisonous.

One potential explanation: Unlike many fruit trees, this species thrives near salt water and I believe its fruit spreads via the ocean. So being toxic to animals did not prevent its spread, and in fact it may be that this is a superior method of propagation, so those preventing ingestion allowed more fruit to float away. I see that other have mentioned this idea, but not in this stackexchange.


text:
Are viruses self-propelled?
So obviously, viruses are nonliving. But when my teacher was teaching viruses in the video (we're doing "flip" learning this semester), the way he described it, it seemed like the viruses responded to their environment in that they moved around until they found a cell of the right type, and then they latched on and hijacked it.
I had always thought of it more like that they were just kind of floating around, carried by the host system (blood in animals for example), until they "bumped into" the right kind of cells and both sets of membrane proteins "docked". But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria.
But, the idea that viruses propel themselves doesn't make much sense either, because viruses are nonliving, and one of the characteristics of life that they do not meet is that living things acquire and use energy.
In summary my question is, how are viruses propelled? Do they move themselves, or are they moved by external forces?

All of your reasoning is correct - viruses are not motile (i.e. not self-propelled).
I don't understand why you think this would cause a difficulty in the case of bacteria.
Edit in response to comment @Remi.b
Some cursory research on estimating probabilities of collisions between particles engaged in random walks has revealed some very challenging maths. So I decided to simply look at some data.
Remarkably there is a fairly recent paper describing investigations of the kinetics of bacteriophage adsorption.

Moldovan, et al. (2007) On Kinetics of Phage Adsorption. Biophysical Journal 93:303–315

I didn't realise it was still possible to publish papers like this, but in fact it is very interesting. For our current purposes we only need to consider the data presented in Figure 3, which show that when E. coli cells at a density of 108 cells ml-1 are mixed with bacteriophage λ at a density of 5 x 104 particles ml-1, then 90% of the phage have attached to a bacterial cell within less than 10 min.
Just to relate this to a real life situation, it is estimated that sea water contains bacteria at a density of 106 cells ml-1 and phage at 5 x 107 particles ml-1.

The OP says "But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria". I think the OP's issue with the fact that viruses are not motile is that he/she doesn't get how they would manage to "find" bacteria (or host cells). One could maybe improve its answer by talking about probability of "finding a new host" and about the behavior (in short) of the virus when it enters in contact with a potential host bacteria.

What do you mean with "I didn't realise it was still possible to publish papers like this"?

It was a bit of a throwaway comment - it seems to me to hark back to the days of the phage group (Delbruck, Luria, Hershey et al), and it is particularly interesting that the authors are physicists (as was Delbruck). As I said, it is an interesting paper, and I certainly didn't mean any disrespect to the authors.

You are right, viruses are neither alive, nor are they moving by themselves. They are moved by passive movements (e.g. the bloodstream or movements of the air) until they meet their target cells. This can be either a cell in the human body (for flu viruses these are cells of the respiratory tract for example) or bacteria (for bacteriophages).
For bacteria both can happen, viruses floating around meet a bacteria they can infect or the other way that moving bacteria meet the virus.

The existing answers are correct. However, there is now one example of a self-propelled† virus.
Herpesviruses assimilate kinesin to produce motorized viral particles

Here, using herpes simplex virus type I and pseudorabies virus as model alphaherpesviruses, we show that a cellular kinesin motor is captured by virions in epithelial cells, carried between cells, and subsequently used in neurons to traffic to nuclei.

Essentially, herpesvirus has been shown to co-opt host-derived kinesin-1 to move from the centrosome to the nucleus along microtubules.
† It’s not self-propelled in the sense that it encodes its own factors to enable autonomous movement, though the described mechanism is more sophisticated than simple Brownian motion. If flagellar chemotaxis in bacteria is analogous to a boat on open water, then kinesin-propelled motion is like a train ride; you are constrained to the tracks.

There are a bunch of viruses that are transported on actin filaments and the like, but this is wild; taking the mechanism with you!! There is so much left to discover in biology.

Wild, indeed!

Viruses move by Brownian motion 1  The definition of temperature is there are an average of about 2 calories (little c) (= 8.3 J) per kelvin, mole, and degree of freedom.  2  Multiply that by 1 mole/6.02E23 molecules and you have the Boltzmann constant (1.4E-23 J/(K*DOF).   So the virus has three dimensions - three degrees of freedom - of physical translation at 300 K room temperature, to get, say, 900 times the Boltzmann constant or 1.2E-21 J of energy.
Which doesn't sound like much, but kinetic energy = 1/2 mass x velocity squared, so if the virus weighs, say, 100,000 daltons = 100,000/(6.02E23) grams, then you divide the joules by this (converting to kg) to get 0.2 m^2/s^2 - take the square root and you have about 0.6 m/s, or about 1.3 miles per hour.
So the virus ambles along at a walking pace (give or take - see the Boltzmann distribution), requiring NO ENERGY to do so.  The caveat is that it has no control over where it goes; this is heat energy.  You might say that the virus, like a stealthy flatus in a crowded room, is an agent of chaos (or at least entropy), on a mission to go forth and spread out.

The term self-propelled requires some finer qualification in the case of bacteriophages. Although bacteriophages are generally carried via Brownian motion, as described in the other answers, in some of them the attachment process exhibits autonomous propulsion. In particular, they may walk on the surface of a bacteria (see modeling video here) and they inject their genetic material with a syringe-like motion. In doing so they dispense the energy stored in the viral proteins during their synthesis and the phage assembly - in other words they remain nonliving entities, unable to acquire energy and convert it to useful work, their motion being a programmed one, like that of a released spring.


text:
Why don't membrane proteins move?
I understand that based on their tertiary structure, intrinsic proteins have hydrophobic non-polar R-groups on their surface and that they 'interact with the hydrophobic core of the cell membrane to keep them in place'.
But how does the hydrophobicity of both the protein and the cell membrane prevent the protein from moving?

Related: Domains in cell membrane

prevent from moving in what direction? Laterally, left-right, or axially, from-into the membrane?

who said they don't move ? how could the do their job without moving (apart from passive and pores) , I believe correct if I am wrong they they do move a lot like breathing

Proteins can move around the membrane.
Most proteins do move within the membrane. The membrane is a liquid crystal and has fluid behaviour. Specifically, this is due to the membrane being in a gel-state. This gel state allows phase behaviour which means that the protein is able to move around on the surface. This results in an effect that is often referred to as the fluid mosaic model.
Proteins tend not to move out of the membrane.
The protein doesn't leave the membrane as a result of the transmembrane helix being very hydrophobic. This hydrophobicity and the hydrophobicity of the lipid tails means that they self-associate. A better way of describing it is that they fiercely dissociate from the water. A molecular dynamics simulation showed that even in simulations the membrane will readily self-assemble as a result of the hydrophobicity.
This is achieved by a few properties of the TMH sequence. There is a large amount of hydrophobic residues like leucine. At either end of the helix are large aromatic residues called the aromatic belt. Further is the electrostatic satisfaction offered by Gunnar von Heijne's famous positive inside rule and the recently identified negative-outside rule present in helices with evolutionary pressure to optimise anchorage.

(Image source: Baker et al., 2017)
Cymer et al. published a study showing the free energies associated with each part of the transmembrane protein helix (figure below). The overall ΔG for a transmembrane helix in the membrane is ~-12kcal mol−1. This means that the association of the helix in the membrane is typically spontaneous.

(Image source: Cymer et al., 2015)

Good answer. A video of proteins in a membrane actually moving is always fun: https://www.youtube.com/watch?v=CfRvmtBdZ9I

No other answer has mentioned this so I created an account just to say this.
Some membrane proteins do not move. This is because they are fixed in that position in the membrane due to the cytoskeleton. Erythrocytes are a good example of this.
The main protein that is immobilised in erythrocyte membrane is Band 4.1 protein, and its immobilised by Spectrin.
Spectrin forms a tetramer(2 dimers together) that acts like a chain/rope connecting membrane proteins and locking them in place.  Spectrin connects to the Band 4.1 protein (also to actin, but less important).
Spectrin also binds to Band 3 protein (via ankyrin, just a protein that connects spectrin to band 3). Band 3 is an anion channel (for HCO3- and Cl-, which is important for red blood cells to function. you want these band 3 proteins to remain evenly spaced out, so they are fixed in the membrane to make sure)

It is important for some membrane proteins not to move. Otherwise the cell will lose its function in some cases(like intestinal epithelial cells), imagine if SGLUT-1 (glucose + galactose transporter) moves from the luminal side(facing lumen) to the basolateral side(the other side)... what do you think happens to its ability to take in glucose from intestinal lumen?
Finally as a bonus, some membrane proteins are also fixed in the plasma membrane in plants (does not move around) by cell wall.
Anyway, if you are bored of someone immediately saying "fluid mosaic model means proteins always move around!" then read my answer

So that's how they do it! Could you add some references so I can go and dig up on these examples further?

There are two types of proteins that are present in a membrane, because you have not been specific about which type of protein you are talking about I will consider that you are talking about Integral membrane proteins.
For more clarity I will begin by explaining to you what are these proteins present in the membrane.
As I said there are two types of proteins 1.

Integral membrane proteins - these are proteins that are present inside the membrane.
Peripheral membrane proteins - These are the proteins present outside the membrane on either side linked through weak electrostatic interactions with the lipids or the integral membrane proteins.

As it is clear from the diagram given below.
 [2]
You have not been clear about which type of protein you are talking about so I assume that you are talking about Integral proteins.
You stated in a nutshell that protein is hydrophilic so it should move out of the membrane as the membrane is hydrophobic. ( correct me if I am wrong here).
You are highly mistaken here. Yes there are R groups present on the protein but when the protein undergoes transitions to secondary and tertiary structure these hydrophilic R groups move to the innermost in the protein structure and hydrophobic groups are outside facing the lipid sea, so they can establish hydrophobic interactions with the lipids.
Integral proteins Do not move out of the membrane because of the strong hydrophobic interactions.
But they do move inside the membrane. As the membrane structure is fluid mosaic. Imagine of proteins as floating in a sea of lipids.
https://www.ncbi.nlm.nih.gov/books/NBK26878/
1 = Principles of Biochemistry Lehninger.
[2] = http://cbc.arizona.edu/classes/bioc462/462a/NOTES/LIPIDS/Membranes.html for the image.


text:
How is it possible for only one in five children to have brown eyes when their parents both have brown eyes?
I have observed that parents having brown eyes had three female offspring with blue eyes, one son with green eyes, while only the youngest daughter had brown eyes.
How can they produce so many blue-eyed offspring?

You directly observed it, why are you asking if it's possible? Also, you should rephrase your question to remove all personal aspects.

Eye colour is more complex than one colour being dominant over the other. At least 10 genes and the relationship between those genes account for many factors including hue and saturation.

I would recommend to "father" to perform genetic testings in question does he related to these children at all.

""My mother," answered Telemakhos, "tells me I am son to Odysseus, but it is a wise child that knows his own father." - Homer, ca 1000 BCE.

My father's father had blue eyes.  My mother has blue-green eyes.  Between the two of them they produced four brown-eyed daughters, all with strong family resemblances.  Probability is only meaningful with a much larger sample set.

Possible...yes of course! The answer could stop there but I guess you want to ask how likely it is.
Here is a chart of probability of a given kid to have eyes of a certain color given the parents eyes color. (Note that the second column contain probabilites and not odds contrary to what the figure is stating).

The probability that $k$ kids out of $n$ have eyes of a color which appears with probability $p$ is given by the probability mass function of the binomial distribution $\binom{n}{k} p^k (1-p)^{n-k}$
Knowing that both parents have brown eyes (even for your oldest sister):

The probability that exactly one out of 5 offsprings have brown eyes (and the others have eyes of another color) is about 0.015 (3 out of 200).
The probability that exactly 3 offsprings have blue eyes (and the others have eyes of another color) is about 0.0021 (2 out of 1000)

You might want to calculate the probability of having $k$ or more kids that have eyes of a given color (a p.value) is obtained by summing probabilities. For example, the probability that 3 or more kids (out of 5) have blue eyes is  $\binom{5}{3} 0.0625^3 (1-0.0625)^{5-3} + \binom{5}{4} 0.0625^4 (1-0.0625)^{5-4} + \binom{5}{5}  0.0625^5  (1-0.0625)^{5-5} ≈ 0.0022$
Learn more about Stats
You'll probably want to learn a bit about statistics if some things are unclear. You might want to make sure you understand the concept of p.value and its interest and make sure you understand what a binomial distribution is. You may also want to understand the concept of multiple testing to avoid falling in simple pitfalls.

Where is that image from?

Hum... I quickly took something from google image. I already saw this kind of image several time and assumed it was trustful. Does it seems wrong to you? There are several images of the kind all showing more or less the same probabilities

@Remi.b Although I agree that they are important concepts I fail to see what does p.value and multiple testing have to do with your answer? As far as I know you are not performing null distribution hypothesis testing, just computing probabilities. (I see the relation for the binomial distribution though).

@Remi.b I'm not saying it's wrong, l just think you should cite your source both for fairness and so people (such as myself) can read more about how the probabilities were derived.

@canadianer ou are right. I'll add a reference if I can find one.

@ddiez multiple testing: Because one can calculate p.value about anything and will be very shocked as soon as (s)he find something that is unlikely to happen. Typically if the OP starts calculating the probability to have 3 or more kids with blue eyes and the probability to have 1 or less kids with brown eyes or the probability etc... p.value: I disagree. I calculated a p.value. I performed a binomial test (exact test) and got a p.value by calculating the probability of something or anything judged more extreme to happen.

@Remi.b p.value is not the same as probability (https://en.wikipedia.org/wiki/P-value). Well, it is a probability but the p.value is defined in the context of hypothesis testing where you test whether you reject or not the null hypothesis. The p.value defines the probability of being wrong when rejecting the null. In that context multiple testing is necessary when performing more than one test.

A p.value is the probability of a given event or any event more extreme to happen given that Ho is true. This is what I calculated. A binomial test is a statistical test (based on hypothesis testing just like any statistical test) and what I calculated is indeed a p.value. Just pick a significance level (0.05 for example) to make your test. If the OP calculate those pvalues for the number of eyes of any color in each family, (s)he will be performing 3 tests (as there are 3 possible colors) and therefore there is an issue of multiple testing. Btw, awesome website @ddiez!

I do not think we agree here :-) Maybe we should discuss this in more length in chat, but I have limited time to visit the site unfortunately! At any rate, your recommendation in the answer is an important one and so from that point of view I have no complaints.

Flashbacks to maths with the binomial expansion... :P

After thinking about it for a while I have arrived to a slightly but important different view on this problem. I will try to explain the statistics behind it to the best of my knowledge. I will use the eyes’ color probabilities in @Remi.b’s response, but of course those may not be accurate and the results can change accordingly.
The problem is to determine how likely is to have 3 children with blue eyes, 1 with green eyes and 1 with brown eyes when the parents both have brown eyes. I will assume each child is independently born (e.g. there are not identical twins). We can use the analogy of a bag with balls from which we draw 5 balls independently.
Imagine you have several bags with $n=100$ balls each. The balls can be brown (M), blue (B) and green (G). Depending on the bag, you will have different proportion of balls. For example, in the bag labelled MM (for brown:brown), there are 75 M balls, 19 G balls and 6 B balls (rounding the probabilities in @Remi.b's answer). The bag labelled GB does not have any M balls (0), and has 50 G and 50 B balls. And so on. This gives us for each bag the probabilities defined in @Remi.b’s response.
Although there are many bags in our particular case we only care about the MM bag, so we should only consider those probabilities. Imagine now you pick five balls at random from this (the MM) bag. What is the probability that you will get $m=1$, $g=3$ and $b=1$ (with m, g and b representing the number of M, G and B balls respectively)? Because there are three types of balls (or categories) this is described by the multinomial distribution (and not the binomial, which describes events involving two categories, like the flip of a coin). The multinomial probability mass function is defined in this problem as:
$$ Pr(M=m,G=g,B=b) = \frac{n!}{m!g!b!} p_M^{m} p_G^{g} p_B^b
$$
Where $P_i$ are the probabilities described above, n is the total number of childs, and m, g, and b are the number of childs with M, G and B eye color respectively. Therefore, for our family we have the following computation:
$$
Pr(M=1,G=1,B=3) = \frac{5!}{1!1!3!}(0.75)^1(0.1875)^1(0.0625)^3 = 0.000686643
$$
The probability (~0.07%) looks very low, but it is basically about 7 out of 10,000 families with parents having both brown eyes and 5 children. Given the large human population it is difficult but not impossible.
Personally, I knew a family where the parents had both brown eyes and the two children had blue eyes. Always wondered about it but this is the first time I actually tried to think about the probabilities! In this case the probability would be 0.00390625 (~0.4%).
BTW, you can easily compute the same in R with the following code:
> dmultinom(c(1,1,3), 5, c(.75, .1875, .0625))
[1] 0.0006866455
> dmultinom(c(0,0,2), 2, c(.75, .1875, .0625))
[1] 0.00390625


text:
How and why are cells irradiated in human-rodent hybrid cell biology?
When human-rodent hybrids are made the amount of human chromosome in the hybrid can be reduced by irradiation. Why and how exactly is this irradiation step performed?

"Why and how exactly is it performed?" Are you specifically asking about irradiation?

Im asking chiefly why it is done

And the principle behind it

I've made an edit that tries to specify that a bit better.

Human cells are irradiated with X rays (to fragment the DNA) and then fused with rodent cells. This is useful for mapping because closely linked markers are more likely to appear in the same hybrid: there is a lower probability of radiation induced breakage between the markers because they are close together.


text:
Did I just watch a spider die?
So I'm sitting in my office and all of a sudden a small spider is gliding down on a web string from the ceiling, right in front of my eyes, and down onto my desk. It proceeds to make a few awkward movements which looked like it was having problems correctly coordinating its legs. Then it flipped on the back and had its legs curled up (like it was dying).
A few seconds later it suddenly started moving with the awkward movements (like it was trying to walk) for a few seconds before collapsing again. It's been doing this on and off about 3 to 4 times. As far as I can tell, the unconscious periods are becoming longer and the waking periods shorter.
What's happening here? Is it dying (of stress / bitten by a female spider / old age) ?
Edit: The whole process has now been going on for over 30 minutes. During the times it moves, it looks like it cannot use the foremost pair of legs. Here are two pictures of the (really tiny) spider with a shopping cart token coin for scale:

Images of the spider and your location will be helpful.

I'm voting to close this question as off-topic because this is anecdotal.

Well thanks @AliceD, maybe you'd also like to point me into the right direction on how to ask this question without being anecdotal?

March Ho made an excellent suggestion. That would help and make it evidence based. Feel free to edit and I'm happy to retract. As of now all we can do is guess. Pointless.

Taking somewhat good pictures took a while, and I'm afraid they won't do you much good as it's really hard to get a good shot of something so small. I hope it helps!

So--did it die?

Appearently, yes. However, it went on for over 16 hours, because when I came in the next day, the spider had moved again. Ever since then, it hasn't been moving again and I'm starting to think that it is really - finally - dead.

However, what kind of agony goes on for 16 hours for this little guy? I would have really liked to know some possible reasons, but it looks like nobody with enough knowledge about spiders is around :)

@AliceD why is this off topic? The underlying question seems to be "what happens when a spider dies"? It seems on topic as far as I can tell.

The mortality rate of spiderlings is very high and their death is a natural process. Since there was no source on energy available on the desk death occurred after stored energy was depleted.

I have just witnessed the same thing occur! The spider (which was in my bathroom) looks to be the same species judging from size and coloration. This seems to me like a natural body process of sorts. At first I was skeptical it could be a sort of infection or parasite, as it was odd that a spider would, by itself, walk into a well-lit area and then roll over to die. However it seems incredibly unlikely that is the case, due to the similarities our spiders share. What are the chances of the same thing happening twice, even if it IS a parasite? Must've died or old age, or venom from another spid

Spiders do curl up their legs when they die. Since they do not have muscles for extending the legs at their joints, they control the haemolymph pressure in the legs by using the blood pressure spike from their heartbeat to extend their legs out or walk. And with no heartbeat (when the spiders cease to exist), they curl up upon death.

Source: http://www.informationsociety.co.uk/why-do-spiders-curl-up-when-they-die/


text:
Does avoiding medication that alleviates symptoms shorten the length of a cold?
People use over the counter (OTC) medications to relieve symptoms of the common cold.
However, these symptoms are part of the immune response, right? They are driven by the body responding to the virus and attempting to make the body less habitable and thus easier to kill it off.
Do OTC medications that reduce cold symptoms cause the cold to persist longer? Should such medications be avoided if the goal is to reduce cold duration rather than symptoms?

It is plausible but by no means established that antipyretics (fever suppressors) in particular could increase the duration of infection/symptoms, because fever is part of a functional immune response.
From Graham et al 1990 (a small [n=56] randomized trial of the use of antipyretic pain relievers in volunteers experimentally infected with rhinovirus):

Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo) ... There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.

In other words, it looked like the people who took aspirin or acetaminophen had weaker immune responses and more cold symptoms. They might have been infectious for slightly longer, but it's hard to tell (also, duration of infectiousness is not the same as the duration of symptoms ...)
However, a review (Kim et al 2013) concluded that NSAIDs (non-steroidal anti-inflammatory drugs) slightly (but non-significantly) reduced the duration of illness.

In a pooled analysis, NSAIDs did not significantly reduce the total symptom score (SMD -0.40, 95% CI -1.03 to 0.24, three studies, random-effects model), or duration of colds ([mean difference] -0.23 [days], 95% CI -1.75 to 1.29, two studies, random-effects model) [emphasis added]

Here is the figure from that analysis:

In medical terms "common cold" means rhinovirus (and possibly coronavirus) infection, but when laypeople might use it to include mild influenza infections (i.e. "I had a cold last week [runny nose, cough, mild fever ...]"). An observational study on influenza A and two other infections (Graham et al 2000) found

There was a striking correlation between antipyretic therapy and duration of illness in subjects infected with influenza A and S. sonnei, but not R. rickettsii ... Multivariate analysis suggested that antipyretic therapy prolonged illness in subjects infected with influenza A, but its use was the result of prolonged illness in those infected with S. sonnei.

In other words, to the extent that one can really distinguish causality in an observational study, it seemed that taking antipyretics made influenza illness longer, but that causality went in the other direction for S. sonnei (i.e., people took more antipyretics when they were sick for longer).
The usual caveats associated with small studies and researcher degrees of freedom apply when interpreting the results of these studies ...

J Infect Dis. 1990 Dec;162(6):1277-82
Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.
Pharmacotherapy 2000 (20), 1417–1422.
(doi:10.1592/phco.20.19.1417.34865)  Effect of antipyretic
therapy on the duration of illness in experimental
influenza A, Shigella sonnei, and Rickettsia rickettsii
infections.
Cochrane Database Syst Rev. 2013 Jun 4;(6):CD006362. doi: 10.1002/14651858.CD006362.pub3.
Non-steroidal anti-inflammatory drugs for the common cold. Kim SY, Chang YJ, Cho HM, Hwang YW, Moon YS.

The Graham trial is still cited relatively often, but it should be mentioned that pooled analysis including Graham shows benefit for pain related symptoms, and no harm or benefit for others (including duration). Graham is also rated as moderate risk of bias. The balance of the evidence for this question (does symptom treatment increase duration of illness) is no, probably not.

Kudos on a supported answer. My only nit-pick is that Influenza (let alone the other two) is definitely not the common cold (and, no, what's true for one virus isn't necessarily true for another.) But +1 for an otherwise nice answer.

both of these comments are good points, I will revise when I get a chance.

@anongoodnurse no virus is the common cold, but influenza infection causes the common cold in 25-30% of cases. The issue with the second reference isn't the fact that it looked at influenza A

@DeNovo - We both know what we're talking about, and what we mean. Let's not quibble like this. Influenza may cause symptoms similar to the common cold, but let's be professional here and assume the OP is talking about infections with rhinoviruses, not strep, H flu, influenza, allergies, or any other etiologies that may present like rhinovirus infections at some point.

@anongoodnurse i don't mean to quibble, but we apparently have a very different opinion of what the common cold is. Though rhinovirus is the most common single cause, half or more of common colds are caused by other viruses, the second most common cause is an influenza infection that doesn't spread beyond the upper respiratory epithelia. The third is coronavirus.

@DeNovo - I understand that it's meant to be a simple question. You're complicating it. That's all I'm saying.

The common cold as a clinical syndrome is not any particular viral infection, but a cluster of symptoms that follow a stereotypical course. It's generally associated with an initial viral infection and you can isolate infectious particles early in the course of the illness, but by the time most people go to the doctor there is no active infection. Because of this, care for a common cold is directed at the symptoms. You could even say (and I do) that the common cold is the symptoms, not the infection.
The development and resolution of many common cold symptoms are unrelated to direct infection. Cough, for example, when associated with the common cold, is not due to infection directly, but reactive inflammation, and is one of the symptoms that lingers the longest. Treatment limiting postnasal drip and, in patients with reactive airway disease, any associated asthma flare up can shorten the length of the illness.
So, no, treating the symptoms in the case of the common cold is not a bad idea, and does not cause the disease to last longer. It may even shorten the disease course.
You can see some of these principles discussed in these clinical practice guidelines  and in this review of the pathogenesis of one of the viruses most often associated with the common cold syndrome.
The general principles in this answer are discussed in Cecil Medicine Ch. 369 and Bennett Prinicples and Practice of Infectious Disease Ch 58. If you're interested in the common cold, I highly recommend reading both of these chapters. Though they were from now dated earlier editions, these chapters really helped me get a grasp on how to approach clinical syndromes in infectious disease when I was starting out.
Note:
See the comments below for valid criticisms of this answer. While the common cold is simple in many ways, good evidence on this syndrome is not simple or common. Host -pathogen interactions are variable at best, and there are thousands of viral serotypes that cause the common cold (many of which cause other illnesses too). My answer here is a synthesis of treatment recommendations and a clinical approach. As @anongoodnurse says, this is probably not a good way to answer a layperson rather than a serious student of human biology via clinical medicine. The summary is pretty simple. If you use medicine that is safe to make someone with a cold feel better, you've taken care of that person's cold.  If you don't have the access or background knowledge to digest Cecil and Bennett, believing this requires you to take an anonymous internet typist's word for it. Because of that, it may not be a good SE answer.

Your links have nothing to do with the OP's question, really, except for "postinfectious". My take on the OP's question is, e.g., "if the first sign of the common cold is a runny nose, does taking a decongestant make the illness last longer?" I don't think this answer addresses that.

@anongoodnurse the key references are the chapters in Cecil and Bennett. I grant that this was mostly a frame challenge. The correct approach is treating the symptoms because the symptoms are the syndrome, not the virus.

@anongoodnurse the reason for the frame challenge is that this is a somewhat common question and an important teaching point. The answer is not a list of meta-analyses of the numerous and varied cold remedies. It's an understanding that treating the symptoms is treating the cold.

You're not teaching med students here, and Cecil is not readily available. Recommending it for a layperson asking a simple question is... I dunno, overkill? Unreasonable? I mean, it's a medical textbook, meant for people training or trained in medicine. I still believe you're off-track with this answer. I'll propose a clarification: Is the virus completely gone once the nose starts running? If it is, that should be made clear. If it's not, that should be addressed with a proper answer.

Lets take this to chat


text:
What does it mean to share similarities among living organisms "both horizontally and vertically"?
I came across the following lines in a textbook (NCERT biology for class 11).

Systematic and monumental description of life forms, brought in, out of necessity, detailed systems of identification, nomenclature and classification. The biggest spin off of such studies was the recognition of the sharing of similarities among living organisms both horizontally and vertically

What does "both horizontally and vertically" mean?

Welcome to Biology.SE! Please [edit] your question to include a reference for this textbook. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

I find it unclear. Maybe "among organisms alive during the same time period ('horizontally') and between organisms and their evolutionary ancestors and descendants ('vertically')" ???

Ben Bolker's comment is correct; the next sentence in the passage helps to clarify (bold added):

The biggest spin off
  of such studies was the recognition of the sharing of similarities among
  living organisms both horizontally and vertically. That all present day
  living organisms are related to each other and also to all organisms
  that ever lived on this earth, was a revelation which humbled man and
  led to cultural movements for conservation of biodiversity.

The relationship between species in the present day are the horizontal relationships; one can define species horizontally by looking at and grouping organisms existing today (or at any other time "slice"). You can compare species horizontally by, say, looking at the skull of a human and the skull of a chimpanzee.
The relationship between species today and species that have existed in the past are the vertical relationships. For example, you could look at the skull of a modern horse and compare it to the skull of Mesohippus.
I've included a couple sources below that use this distinction, though I'm not sure where it originates.
I'd say the "horizontal" terminology comes up more frequently and may be more familiar, for example in reference to horizontal gene transfer one is talking about genetic material moving between species living at the same time. "Vertical gene transfer" can also be defined as the transmission of genetic information from parent to offspring, but more typically you would just call it inheritance.

Alvarez-Venegas, R., Sadder, M., Tikhonov, A., & Avramova, Z. (2006). Origin of the bacterial SET domain genes: vertical or horizontal?. Molecular biology and evolution, 24(2), 482-497.
Stamos, D. N. (2002). Species, languages, and the horizontal/vertical distinction. Biology and Philosophy, 17(2), 171-198.

although in the OPs case horizontal relatedness is not being assumed to be due to horizontal gene transfer, but just due to inheriting genes from a common ancestor.

@John Yes indeed, I'm just giving another example for where the "horizontal' term is used to refer to organisms existing at the same time.

Horizontally refers to organisms alive at the same time, All living organisms share similar genes.
Vertically means into the past and presumably future. How both fossils and genetics show relationships between ancestors and descendants.

Basically the sentence is saying When you study biology and how organisms relate to one another, you see massive amounts of organized similarities in organisms both backwards through time and in extant animals inherited from common ancestors. these similarities form a predictable pattern best explained as a complex web of relatedness stretching backwards in time.
When you realize these and a lot of taxonomic terms originated from paleontology and thus ultimately geology, in which organism relationships were discussed before genetics were even discovered, it makes more sense. phylogenetic trees would have been overlaid on geologic sections. Horizontal groups were organisms in the same horizontal layer of rock thus presumably alive at the same time, vertical meant vertical depth in the rock which was of course different time periods, the deeper you go the further back in time you went. It is a poor choice of wording for a textbook, the less jargon the better, but completely normal in the scientific literature.
here is an example of one of those early combined geologic, taxonomic "trees"

http://museum2.utep.edu/mammalogy/systematics1.htm


text:
does more biomass mean more energy?
I am a high school student and I am very confused about ecological pyramids. My textbook states that the biomass of zooplankton in an aquatic ecosystem is more than that of phytoplankton (I don't know why?) But if I just memorize it then I think that their energy pyramid should also be inverted because more biomass would mean more organic matter {food} and hence more chemical energy available to the next trophic level. This should be true if we are considering all organisms present at a trophic level and not a single organism at each trophic level, right? So why is the energy pyramid always upright? Shouldn't it be the same as the biomass pyramid?
Please explain in simple language using examples; it would be very helpful.

Can you please provide a quote or other source? I suspect you might be misreading your textbook, since phytoplankton is so incredibly abundant.

tl;dr I think you're right and your textbook is wrong. It would be interesting to know (a) what textbook this is (maybe it's the same as the one I quote below?) and (b) what your teacher says if you ask them this question.
In general the energy content of a trophic level is roughly proportional to its biomass (although in going from terrestrial plants to animals we might expect the energy/gram to increase, since terrestrial plants contain a lot of energy-poor structural material). Both energy and biomass would also be proportional to numbers if individuals in each trophic level were approximately the same size (this can go in either direction; whales are much bigger than the plankton they eat, beavers are much smaller than the trees they eat ...)
For oceanic phytoplankton and zooplankton respectively, some reasonable mass/energy conversions are phytoplankton: 2-3 calories per milligram (cal/mg) dry weight (Platt and Irwin 1973); zooplankton: 3-9 cal/mg dry weight (Davis 1993). (ZP are about 3x more energy-rich than PP.)
In my view energy pyramids as well as number pyramids can be inverted, despite what this open-source biology textbook (ref below) says:

Pyramids of energy are always upright, since energy is lost at each trophic level; an ecosystem without sufficient primary productivity cannot be supported.

As detailed below, I think this statement is wrong. The energy loss tends to make energy pyramids a little bit less top-heavy than biomass pyramids, but they can be inverted for exactly the same reason that biomass pyramids can.
The book shows an inverted biomass pyramid:

And explains it as follows:

However, the phytoplankton in the English Channel example make up less biomass than the primary consumers, the zooplankton. As with inverted pyramids of numbers, the inverted biomass pyramid is not due to a lack of productivity from the primary producers, but results from the high turnover rate of the phytoplankton. The phytoplankton are consumed rapidly by the primary consumers, which minimizes their biomass at any particular point in time. However, since phytoplankton reproduce quickly, they are able to support the rest of the ecosystem.

This argument should apply equally well to energy.
In other words, the amount of biomass or energy present in the lower trophic level (phytoplankton) at any moment in time (also called the stock or standing stock) is less than the energy present in the upper trophic level (zooplankton), but the flow of energy is constant (minus losses due to conversion inefficiency).
In particular, if we take the English Channel values (4 g dry mass/m^2 PP; 21 g/m^2 ZP) and convert (g/m^2 * (1000*cal/mg) = cal/m^2) we get at most 3*4*1000 = 12000 cal/m^2 for PP and at least 3*21*1000 =  63000 cal/m^2 for ZP, so the pyramid is still inverted. (In fact, since ZP are generally more energy-rich than PP we would expect the energy pyramid to be more top-heavy than the biomass PP; here I have used the most conservative numbers possible, the top end of the range for PP content and the bottom for ZP content, which happen to be the same.)
For example, suppose individual phytoplankters (yes, that's the word for an individual organism in the phytoplankton) and zooplankters are the same size/contain the same amount of energy (not true, but an OK simplification here), and that there are 10,000 phytoplankters and 90,000 zooplankters per cubic meter of water. The phytoplankters reproduce so fast that each ZP can eat 10 PP over the course of its lifetime without depleting the PP population. In one ZP generation (= 10 PP generations), 100,000 units of energy come into the PP (through photosynthesis) and are eaten by ZP (with a 10% loss due to trophic inefficiency); that's enough to maintain 90,000 zooplankters.

Ecosystems. (2021, March 6). Retrieved September 3, 2021, from https://bio.libretexts.org/@go/page/12640
Davis, Nancy D. “Caloric Content of Oceanic Zooplankton and Fishes for Studies of Salmonid Food Habits and Their Ecologically Related Species.” Fisheries Research Institute, University of Washington, 1993. https://digital.lib.washington.edu/researchworks/bitstream/handle/1773/4192/9312.pdf?sequence=1.
Platt, Trevor, and Brian Irwin. “Caloric Content of Phytoplankton.” Limnology and Oceanography 18, no. 2 (1973): 306–10. https://doi.org/10.4319/lo.1973.18.2.0306.


text:
Bacterial Growth Formula
What are the units of $N$: the colonies of bacteria or the viable cell count?
This is in regards to the bacterial growth formula used during serial dilutions,
$$
N =N(0) e^{kt} \quad .
$$

Either; they're identical to the units of $N(0)$.  In $N =N(0) e^{kt}$,

$t$ has units of time (days, minutes, whatever you have chosen)
$k$ has units of (1/time) (inverse of $t$'s units)
$kt$ is thus unitless, as is $e^{kt}$
$N$ and $N(0)$ have the same units.

If $N$ is a number of something, like anything that is just a number, it is dimensionless and unitless, or with dimension and unit 1.
Note that in chemistry, the "amount" of a substance is not dimensionless but of dimension "amount of matter", with the mole as unit. It is however connected to the number (dimensionless and unitless) of elementary entities in this substance (whether they are atomes, molecules, etc.) through the Avogadro's constant ($N_A = 6,022 140 76 × 10^{23}$ mol$^{–1}$).
However, if your question is whether $N$ and $N(0)$ count the number of individual cells or the number of colonies, I think there is some confusion in your question as the number of colonies (after plating) is a proxi for quantifying the number of viable cells at the moment of plating. But you cannot apply the formula directly to the "number of colonies" since once plated this number will not increase exponentially but stay constant. So $N$ and $N(0)$ refer to the number of (viable) cells.


text:
Worm found inside of wahoo
A fisherman from Hawaii wrote the following:

This Fat juicy worm lives inside of every Wahoo that I catch. Inside
  the stomach. Right at the junction to the intestines. Sometimes there
  are two.

What is this parasite?

It is Giant Stomach Worm (Hirudinella Ventricosa).
It is a platyhelmith parasitic to Wahoo fish, feeding on its blood and found inside the stomach. It makes 98% of Wahoo's parasitic infections.

It is a fleshy worm that varies in size and shape; with extended worms the size of a mans finger and contracted ones about the size of a walnut.

It requires two hosts to complete its lifecycle; a snail and a wahoo fish.
A picture from National Geographic Society
Source: lahaina news
Note: A youtube video shows this worm moving.