In order to form a hybrid, substantial genetic similarity between the organisms is required. To understand why, the successful formation of a zygote from the gametes of the two parents (i.e. fertilisation) in higher animals like mammals requires that the genomes of the organisms be reasonably similar (or homologous; see for instance human fertilisation). This is because successful development of the fetus appears to require that a very specific combination of genes and proteins be present and in the right relative ratios (it's helpful to remember that the genome is a highly analogue computer (see here also), not just a set of instructions to build an organism) - think of the significant effects of simply having an extra copy of one chromosome in Down syndrome, or the fact that triploidy or quadruploidy are often tickets to the death of the human embryo (and so having half of your genome from two different animals could lead to an imbalance in the proteins required to develop normally). I'll be addressing mainly the feasibility of obtaining a hybrid at all; of course in order to become widespread a hybrid would need to be fertile (although see the sterile mule) which would require even more genetic similarity, specifically in order that the chromosomes from each parent can interact, they have to be similar enough that the proteins regulating this process will recognize them as homologous, and enable a process like chromosomal crossover to take place during the meiosis occurring in gametogenesis.

To answer your question about felinae and panthera first, several panthera genomes have been sequenced, and (see here) the tiger for instance has only 95.6% similarity with the domestic cat and diverged 10.8 MYA. For comparison, human and gorilla have 94.8% similarity and diverged 8.8 MYA, so that puts into perspective why you wouldn't expect a tiger-cat hybrid, or for that matter any felinae-panthera hybrids. Those dates are from the linked paper. (Edit: It appears from wikipedia as referred to by the OP above that there actually is a puma-leopard, i.e. felinae-panthera, hybrid which I wasn't aware of (although all of the reports are old, so there is no genetic evidence to prove that it was in fact a hybrid). I assume this may be an exception to the rule; what I was trying to show is why such hybrids are not necessarily to be expected, and as I said below, I'm more surprised about how many hybrids are possible. It does appear though that this particular hybrid is prone to dwarfism, which indicates that it probably does not have a particularly viable genetic makeup, and I think it was sterile).

With regards to your question about felinae hybrids, if you go to Timetree, then it will tell you that Panthera tigris and Felis catus (domestic cat) diverged 14.4 MYA, and by comparison Aciconyx jubatus (cheetah) and Felis catus diverged 9.4 MYA, so it seems reasonable to suppose that they can't hybridise. (But note that P. tigris and P. leo still diverged 6.4 MYA and they can hybridise: the relatedness of two organisms isn't the only thing at work, and a better measure is the genetic similarity; this paper mentions that hybridisation ability correlates both with genetic similarity and time since divergence). Interestingly, this paper actually indicates that the percentage alignment of the cheetah genome to the domestic cat genome is only 91.1% with 93.6% similarity to the tiger, indicating that the cheetah may be a specialised outgroup.

For a more familiar comparison to all of these, Canis lupus which is the ancestor of the domestic dog, dingo, and the gray wolf only arose around 700,000 YA according to wikipedia, although I do not know the exact sequence similarity. Domestic dogs (everything from chihuahuas to great Danes) only diverged 40,000 YA, so the different cats are only superficially similar by this comparison.

There's a diagram on wikipedia shown below which nicely illustrates the different hybrids within felinae (although some seem dubious), so you can see there are actually quite a lot, and although most of the cats involved haven't been fully sequenced, presumably some of these hybrids cross some of the boundaries which I've mentioned above. They do actually include a successful hybrid between a domestic cat and an ocelot (although I can't find another source for this, so it might not be possible), and a hybrid with a jaguarundi (which appears to be closely related to the cheetah) is described as dubious here. Unfortunately, I don't know if either of those cats has been completely sequenced. Ultimately predicting hybridization is a complicated field.

This image below shows a more detailed phylogeny of the cats to illustrate the evolutionary timescale:

And for a comparison to all of that, this image below (from here) shows the phylogeny of the dog (which you might be more familiar with in terms of hybridisation), and if you realise that the whole part of the tree in B from the bush dog down diverged 9-10 MYA (see here - comparable to the whole cat family) and that the bush dog despite its name is extremely dissimilar to modern dogs (for instance it only has 74 chromosomes compared to the domestic dog's 78), then this will illustrate that the evolution of the modern hybridisable dog family (in C in the image) is tightly packed into a much much shorter time than the entire cat branch. All of the names like D1 on the right are modern dogs.

With regards to your question about artificial creation, I think a point to remember is that a lot of these cats are rare/endangered and although such hybrids are still done, there is also criticism of such proceedings. Anyway, I think a good take-home point is that the cat family is actually very genetically old and diverse. I think it's more surprising how many cats can actually be hybridised.


Why does methylation not occur in viral DNA?

Contrary to the question title, viral DNA can be methylated.  See for example Bonvicini et al. 2012. (1) and Hoelzer et al. 2008 (2).

Hoelzer et al. give a review of the presence and role of cytosine methylation in DNA viruses of animals:

  To understand the impact of cytosine methylation on the viral life
  cycle and the evolution of base composition, the particularities of
  each virus will need to be considered. Differences will inevitably
  exist between actively replicating viral DNA and that which is
  integrated into the host genome. The type of viral persistence will
  also be of importance. The integration of adeno- or polyomavirus DNA
  into the host genome is usually a terminal process since the viruses
  cannot liberate their genomes and are therefore no longer infectious.
  The evolutionary roles of methylation in these cases will likely
  differ from those seen in other viruses, such as Herpesviruses, which
  can liberate their genome after periods of latency. But differences
  may also exist between large and small viruses—with many larger
  viruses encoding their own replication machinery and additional
  proteins which modify host cell processes and immune responses. The
  susceptibility of the viral genome to methylation and immune
  recognition will also be affected by other factors, such as the
  location of replication within the cell and the specific intracellular
  trafficking route.

Viral DNA methylation has mostly been studied in large DNA virii, and the extent of methylation may be related to repression of viral replication. Bonvicini et al. writes that

  Epigenetic mechanisms, and in particular the impact of cytosine
  methylation at CpG dinucleotides on the viral life cycle have been
  mainly studied for viruses that can establish latency and undergo
  reactivation, such as viruses in the Herpesviridae family, or for
  viruses that can integrate their genome into the host genome such as
  Retroviridae or Papillomaviridae. In general, a correlation has been
  found between the extent of CpG dinucleotides methylation of viral
  genomes and viral quiescence [24]. Scarce information is on the
  contrary available on the possible occurrence and role of methylation
  for actively replicating viruses


Are high sounds worse for your hearing than low sounds?

Yes.  http://american-hearing.org/disorders/noise-induced-hearing-loss/#causes  Most of the discussion of noise-induced hearing loss talks about the loudness of the noise, only rarely mentioning that higher-pitched noise is more damaging.  Probably because it is much easier to measure the amount than the frequency.


Does the human eye’s field of view shrink when focusing on far away objects?

The lens does flatten when contracted to look at far objects. This is however still a regular cylindrical lens. It's not perfect (even when corrected), but close to it. Straight lines project to straight lines on the image plane (for your eye the retina).

A fisheye lens is different because it creates strong geometrical distortions. A straight line will appear curved on the image plane. You can see that on the images taken below (from some random source). Left is a regular lens, right is a fisheye lens.

The human eye actually introduces some so-called barrel distortions (so it's a little bit like a fisheye lens). You can demonstrate that by looking at this checkerboard pattern (from Helmholtz's treatise on physiological optics). If your eye is close enough you'll see the checkerboard straight, because the barrel distortion introduced by your eye will "straightens" the distorted checkerboard.

Focusing at different distances will make objects appear sharp. Because all light rays coming from this object will project at the same point on your retina. Objects at a different distance will appear blurred because light rays will project at different points causing a "spread" (defocus blur, see image from wikipedia "circle of confusion" article). This is however totally independent from the field of view. Test it yourself: take a pen, place it close to your eye. Pay attention to an object far in your periphery, nearly outside your field of view. Now focus to the sky behind the pen (~infinite focus distance), then your pen. In both cases you can still see the object in periphery because your fov hasn't changed.


The body indeed uses lateral inhibition / surround inhibition. When using a muscle, neighbouring muscles are sometimes activated to. So active muscles are excited while nearby muscles are (partially) inhibited (Beck and Hallet 2011)

This surround inhibition is true for fingers (Sohn and Hallet 2004).


Assuming you have stated the question correctly, the answer key is incorrect for exactly the reasons you have given and your reasoning and consequent answer are correct.

I would double-check you have read the question correctly and then conclude the answer key is incorrect. It happens.


Does the anatomy of our hand result in (computer) mouse-accuracy that varies by direction of movement?

Assuming the case where you move a mouse left and right with the wrist and up and down with the fingers, then yes, finger movements are more precise. The fingers and facial musculature are body parts with the most exquisite fine motor-control. The wrist, on the other hand, probably less so. The wrist is definitely involved in fine motor skills such as writing, but the fingers even more so.

I wasn't able to find a good reference about the level of precision for different body parts at the behavioral level. I can, however, approach the question from a neurophysiological point of view. The amount of motor control available for different body parts can be visualized by means of a motor homunculus. The motor homunculus shows how many neurons are available in the cortex for a given body part. The larger the cortical surface dedicated to a body part, the larger the corresponding body part is presented in the homunculus (Fig. 1).

Fig. 1. Homunculus drawn on the motor cortex (left) and the homunculus presented as a figurine (right). Sources: Conference on Human factors (1997) and Autism Index, respectively.

The fingers have a huge amount of motor cortex dedicated to them compared to the wrist. There are a lot of 'buts' to add, most notably the larger number of muscles in the fingers versus the wrist, which explains part of the difference. Nonetheless, the homunculus does show the relative functional importance of the fingers in motor processing power of the brain, while the wrist is virtually invisible on the homunculus (Fig. 1, left panel).

Lastly, you seem to be mixing up 'distance' and 'precision' in your question. While the wrist may cover a greater distance, it is not because of this that the precision is smaller. The fingers have more neuronal processing power behind them and can be exquisitely fine tuned. In other words, the precision is not determined by the dynamic range (distance), but by the processing power dedicated to the motor function.

As a side note, because of RSI, it is recommendable to use gross arm movements instead of fine wrist and finger movements.


Why X-chromosome linked diseases happen due to recessive gene?

First of all, most observed mutations are recessive (see the answer to this question; in brief: homozygous carriers are strongly selected against, heterozygous carriers are not affected only if the allele is recessive). So you wouldn't be surprised to find the same pattern on the sex chromosomes.

A good way to think about the specialty of recessive alleles on the X chromosome, is to think about why these diseases are most often visible in males (and you are on the right track there) ... Most alleles causing heavy disease - be it a mutation on the autosomes or the sex chromosomes - are rare (it is for the same reason they are recessive which is described in more detail in the answer linked above; it is due homozygous carriers being affected by purifying selection again) and therefore female carriers are most likely heterozygous and therefore healthy. In males, however, a carrier is always affected by the disease because the carrier is hemizygous.


When is the lactase in lactose-free milk active?

Having done an inordinate number of rather mind-numbing A.S. practicals involving milk and enzymes the year before last, in my experience lactase always began breaking down the lactose immediately and converting a boiling tube worth of milk in less than 50 minutes at below room temperature.

To further allay your concerns, this website suggests that most Lactose Free milk has undergone UHT treatment - therefore cooking shouldn't be a problem as the enzymes have presumably been added before the pasteurisation, and are therefore denatured - I can't see why you'd then go to the extra trouble of adding the lactase aseptically after pasteurisation; and if the lactase shows in the ingredient list it presumably wasn't done with immobilised enzymes in the factory.


How does a bacterium age without cell division?

First of all, the growth of a bacterium is associated with an increase in cell biomass.So if a bacterium is restricted from replicating it does not grow. Coming to your later parts of the questions about how long will it live and will it age;
Yes, a bacterium would age irrespective of its ability to replicate.According to The Free radical hypothesis, all organisms age due to random deleterious events, oxidative damage by ROS produced during normal metabolism. It has also been found that cells undergo irreparable damage which can also lead to cell death eventually.

A complete review on bacterial ageing:
http://www.ias.ac.in/article/fulltext/reso/017/04/0347-0364


Are intestinal and pancreatic lipases different?

Pancreatic lipase and intestinal lipase are almost same in their functions. In the intestine, the name of the lipase is a triacylglycerol acyl hydrolase it also called colipase dependent lipase or Pancreatic lipase,  Free fatty acids, and 2-monoacylglycerol are the primary products of lipid digestion in the jejunum. and Pancreatic Lipase also produces Free fatty acids and 2- monoacylglycerol.
so we can say that both enzymes are almost same and produce the same products.
Sources Lippincott's Illustrated Reviews Biochemistry 5th edition Chapter 15


Based on the location and picture I believe this a Spotted Sandpiper (Actitis macularis) chick. Once they hatch, they are out of the nest, the one you are holding looks fairly small still, must have hatched recently.

You can find more information about them here.


difference between motifs, domains, patterns, signatures and profiles

Looking at the documentation you provide, I think that I can provide definitions for those terms as defined by EXPASY. Note that those definitions may just be an in-house system that EXPASY uses that you can't generalize to other databases for instance.
First, in section I.C of the documentation, they write "The use of protein sequence patterns (or motifs) to determine the function(s) of proteins is becoming very rapidly one of the essential tools of sequence analysis."
So it looks like for them patterns = motifs and motifs = patterns. Note again that "pattern" appears to be a somewhat informal term. I would certainly say that it is confusing that they use them as synonyms, but they do at least define them as such.
Second, I think that they are using the word "profile" in a very narrow technical sense, with regard to the way that they detect homology between proteins. The standard way to detect homology between proteins is using programs called Hidden Markov Models (HMMs). In section II.B, they write "A profile or weight matrix (the two terms are used synonymously here)...". So a profile is really just a weight matrix derived from a HMM that can be applied to any given alignment to figure out whether or not it matches homology. They go on to give an example of how this weight matrix is applied.
In simple terms, how the HMM works is that you give it a bunch of sequences that you know belong to the same family, and it will try to learn the frequencies of amino acids at each position and what order they come in. This model of the amino acid frequencies is the weight matrix they talk about. Then you make sure that the HMM works well (gives high scores for proteins in the same family, low scores for proteins in different families), and then you can apply the program to try to find new homologs.
Hope that answers the Q.


Does an old growth forest ecosystem produce more oxygen than it consumes?

Does an old growth forest ecosystem fix more CO2 than it produces?

The intergovernmental panel on climate change summarizes some of the data on carbon flux here. For the amazon similar tropical rain forests, it says:

  Measurements in pristine, seasonal tropical rain forests in Amazonia indicate NEP of approximately 1.0 t C ha-1 yr-1 (Grace et al., 1995a,b) and approximately 2.0 and 5.9 t C ha-1 yr-1 for dense, moist rain forest (Fan et al., 1990; Malhi et al., 1998, 1999).

NEP is net ecosystem production, which, as I understand it, is essentially the total amount of carbon fixed by the ecosystem.

It seems the tropics, and the Amazon, in particular, are important global carbon sinks. This is also discussed in this more recent article in Nature.

This isn't my field, but as far as I understand it, forests are not closed or steady state systems. They do play a role as a sink in the global carbon cycle. I would assume net carbon fixation must come with increased biomass, so I may have just avoided a key part of your question. All the same, I think the point is that, again, even the amazon rain forest is not at steady state.

As far as oxygen is concerned, the report and article don't address it. I suspect this is because there is no documented problem with global oxygen depletion.


Exactly what biochemical factors control the intensity of an allergic reaction?

Network of possible factors that contribute to the variability of the immune reaction between individuals is still not well investigated.

Type I hypersensitivity is mediated by IgE antibodies, which means that lymphocytes B after initial contact with antigen undergo oligoclonal selection. Only these with the highest affinity towards the antigen will survive. During this process (see: germinal centre reaction) genomic regions responsible for antigen binding change their sequence in non-deterministic manner. So, each individual has slightly different set of antibodies targeting the same antigen.

Moreover, within the same antigen (allergen), different regions (epitopes) can trigger the immune reaction in different individuals.

Other, more general factors also contribute to the symptoms associated with hypersensitivity reaction. For example: hormones, infections, medications, microflora condition, genetics (eg. major histocompatibility complex) or even psychological status.

Also see:
Article 1
Article 2
Article 3


Are pulp cells (in oranges) normal plant cells?

They are not individual cells. In fact, the "juice sacs" (as they are known) are actually specialized, multicellular hairs:

  Juice sacs originate as multicellular hairs in which the interior of the enlarged distal part breaks down and fills with liquid. The juice sacs constitute the fleshy, edible pulp of an orange and are the source of the sweet juice.

(Quote and image from Fruit Terminology, palomar.edu)

This is from a botany course; if for some reason that isn't reputable enough, check out the book Anatomy of Seed Plants by Katherine Esau (1960).


Is it technically possible to make someone see something when their eyes are closed?

Yes, this is most certainly possible and already being done. As long as the visual cortex of the brain (in the occipital lobe, i.e. at the back of your head) is functional, the correct stimulation will produce visual perception.

In cases of blindness caused by malfunction of the retina, meaning that the rest of the visual pathway is functional, this is the most promising approach to restoring vision. See Visual prosthesis and the TED talk on it.

"Virtual vision" as in projecting a whole field of vision (reflecting the real surroundings) is the big ideal target that this technology is aiming for. Of course as soon as they manage to make a working prosthesis for blind people, someone will probably try to make it non-invasive and easily usable for commercial exploitation.


What organs are absolutely needed by the human body?

You can't remove most organs. The heart, lungs and brain are the ones that without you'll die in seconds. The rest you'll live a few hours or more. All depends how long you wish to live. The best way to see which organs are most required is to look at the order organs are shut down when there isn't enough oxygen or blood. That tells you which area most and least important.


There seems to be no effect of vitamins. This paper ("Preventing cognitive decline in healthy older adults." found no evidence for herbal supplements, vitamins or fatty acids improve cognitive functions.

There seems to be some evidence ("Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.") that a cocktail of hig dosed vitamins including folic acid, Vitamin B6 and Vitamin B12 can slow Alzheimer's disease. But: The benefits were only seen in participants which had high blood levels of homocysteine. This amino acid is linked to a higher risk of heart disease for which the B vitamins are postive for the outcome. So this might only be helpful for people with too high homocysteine levels.

And its questionable if high doses of antioxidants (like vitamin A or E) are not only not helpful, but can cause actual damage. This is due to the fact that they catch up reactive oxygen species, which might otherwise trigger the cell to go into apoptosis and prevent it from becoming a cancer cell. Here is the paper: "Antioxidants accelerate lung cancer progression in mice.".


What species of flying insect is this? Resembles a fly with the wings of a dragonfly

Insect ID from photos is difficult, but this is definitely in Syrphidae. The alternating thick and thin stripes on the abdomen resemble very much those in a picture I found here: https://alchetron.com/Episyrphus-balteatus
I would say that it is likely in the genus, Episyrphus, which is present in Austria.


Is there a standard format for plant community composition data?

There does not appear to be a current standard, but Veg-X is a standard that has been developed to facilitate exchange of plot-based vegetation data, and may provide the closest to what you are looking for.

Veg-X is described in Wiser et al 2011 and the project home page is http://wiki.tdwg.org/Vegetation/

From the abstract:

  The exchange standard for plot-based vegetation data (Veg-X) allows
  for observations of vegetation at both individual plant and aggregated
  observation levels. It ensures that observations are ﬁxed to physical
  sample plots at speciﬁc points in space and time, and makes a
  distinction between the entity of interest (e.g. an individual tree)
  and the observational act (i.e. a measurement). The standard supports
  repeated measurements of both individual organisms and plots, allows
  observations of entities to be grouped following predeﬁned or
  user-deﬁned criteria, and ensures that the connection between the
  entity observed and taxonomic concept associated with that observation
  are maintained.

Wiser, S.K., N. Spencer, M. De Caceres, M. Kleikamp, B. Boyle, & R.K. Peet. 2011. Veg-X -- An international exchange standard for plot-based vegetation data. Journal of Vegetation Science 22:598-609.


From an information perspective, are both strands of DNA necessary?

From a strictly information theoretical perspective, no, a second strand does not provide any additional information that cannot be inferred from the complementary strand. But as many comments have pointed out, there are many practical reasons for DNA's double strandedness.

DNA is biochemically more stable in a double stranded state.
The redundancy of two strands allows for maintenance and repair mechanisms to ensure the integrity of the genome.
Proteins that bind to DNA can only recognize the sequence of that strand, so even though the complementary strand can always be reconstructed from the primary strand, DNA binding proteins cannot target that complementary strand unless it physically exists. In some cases, a DNA binding site encompasses both strands simultaneously.
Proteins (such as polymerases) traverse DNA in the 5' to 3' direction, so if information from the complementary strand was required it would have to be read "backwards".


How are chemical reactions organized in prokaryotic and eukaryotic cells?

Okay, this is my first post on this site so please bear with me when it comes to the format of my response!

To begin with I'm going to try and answer your question by clarifying some things.

  In prokaryotic cells I thought there were no
  organelles so does that mean that every reaction depends on the
  diffusion of the reactants throughout the cell and that any reaction
  could happen anywhere in the cell?

Yes and no, the fact that there are no membrane bound organelles in prokaryotic cells means a majority of the reactions occur in the cell's cytoplasm via diffusion but something to keep in mind is the selectiveness of the cell's membrane will regulate the substances entering the cell in turn controlling that reactions that occur within it.

  What I'm getting at is that if everything is just floating around
  freely within a cell, wouldn't a lot of reactions interfere with each
  other?

When it comes to  eukaryotic cells structures do not float around freely like soup, there is cytoskeleton composed tubules and filaments that is used for  intracellular transport, this skeleton acts like a road system to move substances between static organelles. Prokaryotic cells do not require this since they do not have membrane bound organelles and the diffusion of substances into the cell is controlled by the cellular membrane.

  in eukaryotic cells, are organelles always used to compartmentalize
  stages in chemical synthesis?

Not always, you can look at things like cellular respiration to see glycolysis occurring in the cytoplasm.

I hope this helped out some!


I think the reason you are having trouble discerning the statement is because it doesn't really make much sense, nor is it in my opinion sufficiently explained in the paper. The sentences preceding the it give a little explanation as to what the author may be getting at:

  So far, 1500 allergenic structures have been identified. Online allergen databases and allergy prediction tools are being used to find cross-reactivity between known allergens. Localization of B and T cells in the allergen may not coincide.

During an exaggerated immune response (allergy) the lymphocytes (B and T) will localize (travel or accumulate at) to the site of the antigen (allergen).

If I could guess I would say the author is stating that data has shown that no immune response is taking place (data generated by assessing the accumulation of lymphocytes near the allergen), despite the fact that these online allergen predictors say that an immune response should be generated.

The statement in my opinion moves to discredit these online allergen predictors.

I did look over some of the rest of the manuscript, and found two other ambiguities within.

The author does cite another paper in your sentence that may shed more light on this:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2686541/?report=reader

An overview of it provided little clarity however.

I fear that only  a crystal ball or this question addressed to the senior author may answer your question with complete certainty:

Dr. Rajat Kumar De
Professor
Machine Intelligence Unit
Indian Statistical Institute
203 Barrackpore Trunk Road, Kolkata 700108, India.


Hybrid vs introgression zone in natural populations

I think you're correct. See Harrison, R.G. and E.L. Larson. 2014. Hybridization, introgression, and the nature of species. J. Hered. 105: 795–809. Also see https://www.differencebetween.com/difference-between-hybridization-and-vs-introgression/

Interesting that you're received no responses to this. It's an interesting (and I think important) question.


Why is chemotherapy-related hair loss temporary?

Most chemotherapy drugs targets DNA replication in some way, which damages not only cancer cells but normal replicating cells as well. But normal cells are typically more resistant, and stand a better chance of survival. It is thought that this is because normal cells respond to DNA damage by "arresting" the cell cycle, and not dividing until the damage can be repaired. Cancer cells, in contrast, have lost these safety mechanisms, and will continue to divide despite having damaged DNA, which can cause serious problems and lead to cell death. This difference is exploited in chemotherapy.

There are of course large variations between individual cells. Some normal cells will die of chemotherapy, and some cancer cells will survive. But statistically, normal cells stand a better chance, and so chemotherapy dosage can be adjusted to a level where the drug effectively kills most cancer cells, but spares at least some normal cells. (Provided the cancer is sensitive to the particular drug used, of course; in many cases this strategy unfortunately does not work.)

After a course of chemotherapy, many normal proliferating cells will also be damaged, causing problems like hair loss and other unpleasant side effects. But given some time, normal cells will recover and repopulate hair follicles and other tissues.


How to calculate the number of folds present in a protein

There are various ways that you could do this.

CATH is a hierarchical classification system
SCOP is another such system with a different hierarchy
PTGL is the protein topology graph library
Tops motif will scan PDB files and match patterns against it

How you actually apply these tools or lookup within these systems is documented on their websites. However, it depends on what you want to do - look up published structures, or new experimental data.

I should point out that writing software from scratch to determine the fold of a protein may be tricky.


Cationic lipid mediated transfection optimization for 150mm dishes

So, for every row on the dish protocol, the entire process is scaled up a discrete value. In the case of 100mm to 150mm, the values are scaled up by about 2.76 across all values:

(a) 152/55 = 2.76, (b) 1.52e7/5.5e6 = 2.76, (c) |avg(30.4-45.6)/avg(11-16.5)| = 2.76

(as answered in comments)


How can dopamine modulate synaptic strength?

Yes, dopamine receptors (D1-D5) are G protein coupled receptors,  which act primarily on adenylatecyclase (changing cAMP concentration, which activate proteinkinase A, which phosphorylates other proteins in turn such as CREB... you can find the pathway in the following article). D1 receptors activate adenylatecyclase, D2 inhibit its activity.

I wouldn't say it directly alters the Ca2+ channel concentration per se, the article says however it can modify their state.

According to this article, G proteins of these receptors could also have different effects (alternative effects through G-proteins such as activating phospholipase C, which results in IP3 formation which results in Ca2+ influx to cytoplasm from ER which acts on proteinkinase C) or new research suggest that it could also act through G protein-independent mechanisms via interactions with ion channels.

  specificity of the location (of the brain) that dopamine acts on controlled?

The idea is that cells with certain neurotransmitter may induce growth of cells with same transmitter, thus forming specific circuits. I don't know however how specifically this happens and how the cells communicate to form specific connections (like dopaminergic connection from substantia nigra to basal ganglia) during development. I'd bet on some morphogenes. Someone else might know better :) .

Yes, dopamine is associated with addiction, as it's part of the reward system in brain. Many drugs inhibit its transport from synaptic cleft into the cells, which means prolonged activity, brain senses positive effects you can see when you've done something good (reward).


Book recommendations for algorithms used in evolutionary biology

What you are describing usually falls under the category of computational biology or just mathematical biology. Unfortunately, the biggest part of this field is bioinformatics, or the application of statistical and/or dynamical programming techniques to sequence data. You exclude this in your question, and I would agree with you that it is a "boring" topic from a theoretical biologist's perspective, because it mostly uses computer science in a very standard way as a tool for experimental biologists.
As you noticed, it is also standard to use computational models in theory papers as a way of simulating things. I think this is the sort of resources you are asking for. Unfortunately, specific algorithms are seldom standardized or reused in this area. Typically, each paper (or sequence of related papers) uses their own models.[1] As you read a lot of papers, you will find some common themes, but these are just standard ideas of theoretical biology expressed as simulation. I doubt that comprehensive books exist, and even if some do their utility is not clear to me due to a lack of specific algorithm (re)use.[2] However, the most commonly used techniques are to either to solve differential equations numerically (which most would classify as mathematical modeling) or run agent-based or population-based models. General resources on these exist, and here are some discussions for the latter other SEs:

Simulation modeling of diseases.
Sources for Algorithmic Evolutionary Game Theory.
Canonical reference on agent-based computing.

Finally, do not confuse 'computational modeling in theoretical biology' with 'algorithmic biology'. Algorithmic biology is a new field that views ecological and evolutionary dynamics as computatioanl proccesses. Instead of using mathematical tools borrowed from physics (as is standard with the dynamic systems approaches to mathematical biology), it uses the tool of theoretical computer science (note that this is a type of math that has very little to do with programming the laptop infront of you). I know of only two books in this field:

Gregory Chaitin "Proving Darwin: Making biology mathematical" - Although Chaitin had contributed significant and original thoughts to computer science in the past, I would strongly advice against this book because it misses the point from both the biological and computer science point of view.

Leslie Valiant "Probably Approximately Correct: Nature's algorithms for learning and prospering in a complex World" - in this book (based on earlier papers), Valiant recasts evolution as a type of machine learning. This is very interesting from a mathematical point of view, although it might not connect directly enough to biologically relevant questions (see also some of the discussion in Kaznatcheev (2013) and Kaznatcheev (2019)) and misses the computational power of frequency-dependent selection (see Kaznatcheev (2020)). But I would recommend reading this book.

Notes

In general, I consider these sort of models as heuristics and I am skeptical of their usefulleness beyond rhetorical devices/examples.
I think that literature reviews would be interesting computational modeling in specific subfields. In fact some colleagues and I have wanted to do this for the smaller area of evolutionary game theory (This answer can serve as a starting point for some algorithmic considerations of EGT).


When the leaf length ranges are given in a plant species' description, what do the numbers in parentheses represent?

Anytime you see this being used in terms of a range...

the numbers outside the parentheses represent the normal or expected range, and

the numbers inside the parentheses represent atypical extensions beyond the normal range that are uncommon but possible and recorded.

Radford, Ahles, and Bell's 1968 flora, Manual of the Vascular Flora of the Carolinas confirms this in its preface (page vii):

In instances where most measurements for a character fall within one part of the total range of variation, the more infrequent or extreme size range is given in parenthesis as an extra measurement: e.g., "leaves 4-8 (16) cm wide", not "leaves 4-16 cm wide."

So, in your example, you can interpret the first range as follows:

Blades are typically 4-5 mm long (but sometimes 6 mm long) and typically 1-1.5 mm broad (though sometimes only 0.5 mm broad).

 Radford, A.E., Ahles, H.E. and Bell, C.R., 1968. Manual of the vascular flora of the Carolinas. Univ of North Carolina Press.


Is this long black insect with semi-long antennae and a large segmented abdomen caught in the kitchen a larva or an imago? And what is it?

That is an adult rove beetle (Coleptera, Staphilinidae). https://en.wikipedia.org/wiki/Rove_beetle
Rove beetles have very short elytra (forewings), so they don't look like other beetles. This one looks a lot like Ocypus olens, which is common in Europe https://en.wikipedia.org/wiki/Devil%27s_coach_horse_beetle


Preventing Diabetes by preventing stress?

Prolonged stress leads to elevated levels of cortisol. Cortisol interacts with insulin action and blood glucose levels in various ways, essentially promoting hyperglycaemia.


I have been trying to read up a bit on this. I started out looking on wikipedia and it seems there are three hypotheses which are not necessarily mutually exclusive.

1.Aid the wicking of sweat away from the skin

2.Reduce friction between the thorax and upper arm

3.Facilitate the release of sex pheromones

The first would seem possible because it would help to prevent over-heating of the lymph nodes under the armpits and that also fits with the fact there are a lot of sweat glands there.

The second, I can't find any citations which support this but I understand that people who shave their armpits tend to suffer from dry underarms. This could be a result of increased friction.

The third is apparently controversial although it seems perfectly reasonable and highly likely to me. There is a famous experiment by Claus Wedekind who got men to wear a t-shirt for a few days. He then got women to choose a most preferred male purely by the scent of the t-shirt and found interesting results relating to the MHC profiles. The armpit hair could help to trap the odour produced by the sweat and help with mate attraction, like some kind of scent sponge. I don't understand why this is so controversial, loads of animals influence mate choice with scent - perhaps people don't like to think we are genetically attracted to each other by sweat because it seems animalistic and less romantic.

In summary, there is no sure answer and it could well be all of the above, or something entirely different.


Are there "multi-frequency" signals within a human brain?

Remembering that neurons don't generate sinusoids, just spikes (mostly)....

It depends on exactly how you want to define "depend on".  For instance, a downstream neuron receiving inputs from two neurons will be more likely to fire as it spatially/temporally sums the inputs from the two neurons.  Regardless of their specific rates, if their interaction is such that an impulse from each neuron arrives within a certain timing of the other, it may be sufficient to cause the downstream neuron to spike.  In this case, particular sets of frequencies of the two upstream neurons would be more likely to activate the downstream neuron and would do so at a particular rate for the downstream neuron.  Of course, the phase delay between the two neurons would be important too.

In a more general sense, one might consider the binding problem, by which many sensory inputs are bound into a single, higher level experience, such as an object or a biographical memory, which can then later be recalled (and thus activate all the lower sensory regions that encoded the memory in the first place, nearly recreating the experience).


How lion can carry the cub without harming it?

The skin of the felines has geneticaly evolved in such a way that the parent can do this.

Its strong and stretchy in the neck area.

Moreover, the cub enters into an obedient state.


Second paper is an article in science Daily and have a pretty decent source from Texas A&M University. It's much better than the first as it is un-sourced post on yahoo answers.

Source:
"Male Seahorses Are Nature's Mr. Mom, Researchers Say." ScienceDaily. ScienceDaily, 2 May 2008.

Why male seahorses gets pregnant?

Genetic answer:

May be because only $MHII\beta$ gene present in the male pouch which carries the babies.

Source and more on this topic:

The impact of sex-role reversal on the diversity of the major histocompatibility complex: Insights from the seahorse (Hippocampus abdominalis)


The Effects of Large Static Magnetic Fields on the Human Nervous System

I don't know anything about long term health effects. The guidelines mentions that noticeable effects begin around 2 Tesla. This is in line with what I have heard. On the other hand, this mentions public exposure limits of 40 milliTesla. Here is a paper from the NIH that discusses health effects of neodynium magnets, but doesn't mention field strength.
Keep in mind that 2 Tesla is an extremely strong field. You are not likely to find it except right next to a large superconducting magnet. Or possibly between the poles of an exceptional research grade non-superconducting electromagnet.
Keep in mind that even if a strong magnetic field has no direct effect on a normal person, it could be harmful to a person with, say, a pacemaker.
Also, a field that strong can turn a stray piece of metal into a dangerous projectile.
Motion in a magnetic field matters because it exerts a force on moving electric charges. $\vec F = q \vec v \times \vec B$. This means for example, a copper wire feels no force, unless an electric current is moving inside it. In people, nerve impules are small brief currents. This may be why people feel effects in large fields. Walking means charges are moving faster.


Are there medical treatments that were so effective they were never subjected to a randomized control trial?

In recent years, clinical trials are all necessary. You have to have the randomised control To make sure it isn't a placebo effect. If and only if the drug seems to be super effective will they cut the randomised control short and give the real drug to everyone.

Sadly, while it may seem unethical, there was a cancer treatment that two cousins got into. The normal treatment guaranteed death, while the new drug actually had people practically bouncing off their death beds. One got the placebo - in this case normal treatment since it's unethical to not at least give standard care - and the other got the drug. The drug worked so well, the doctors tried to push to cut the trial short but they wouldn't and the one on the normal treatment died.

This drug was PLX4032.

blogspot uproar

clinical trial information

NYTimes article

So to my knowledge about clinical trials, no trial has been able to skip that stage. It's actually Called Phase III testing of the drug, followed by Phase IV which is administration to the public. It can, however, be shortened if it is promising enough.


What is the largest perennial herbaceous plant?

As mentioned above, the largest perennial herbaceous plant is indeed the banana.  Whilst the main reference to this ("Yes, we have more bananas" - an article in the Royal Horticultural Society Journal from May 2002) has been removed from their website it would be I'm sure possible to order should you need to.

This summary of the banana mentions that the pseudo-stem of the banana plant grows to 6-7.6m in height - I haven't found anything taller when looking around so it doesn't generate any reason to doubt the removed article.

Regarding the comments on Bamboo, there are 7 genera containing bamboo species.  All of these (Arthrostylidium Rupr, Bambusa Schreb, Chusquea Kunth, Dendrocalamus Nees, Phyllostachys Siebold & Zucc., Pseudosasa Makino and Sasa Makino & Shibata) are described as having persistent woody stems so don't meet your herbaceous requirement.


What to do if microarray t-test, ANOVA, SAM and LImma show various selected significant genes?

I wouldn't expect different methods to give the same results. Further, why are you even testing non-normalized datasets, the results of that are completely and utterly useless for any purpose other than showing that normalization is important. In addition, an T-test is a special case of an ANOVA (and of course limma is itself using a moderated T-test, though it's going to have significantly more power than the others), so I have to ask myself exactly what sort of design you're using that it's appropriate to substitute one for the other and still get apparently vastly different results.

In general, I would strongly encourage you to work with a local bioinformatician or statistician for what is presumably your first microarray analysis, particularly if you don't have a strong statistics background.


Resource for model organism anatomy/physiology for biological experiments

In the Bgee database, you can look at gene expression and anatomy of various model species, e.g. Drosophila. This doesn't give you the full anatomy, but at least an ontology of tissues and cell types.


It's possible, but very unlikely.  Usually it takes a substantial number of genetic differences to qualify two organisms as different species.  One might think that reversing the direction of selection pressure could reverse a genetic change, but genetic change begins with random mutations which are not determined by selection pressure.  It's very unlikely for one random process to undo another random process (imagine mixing black and white sand in a jar by shaking it, then trying to unmix by unshaking!).


There are small parts between Genes in an Operon that does not encode for any amino acids. What is the purpose of these parts?

The regions between the genes on a prokaryote operon are transcribed into the messenger RNA  but are not translated into proteins.  Because they are not translated, they are characterized by the general term UnTranslated Regions (UTRs).  A typical operon having two genes is shown in this diagram from Wikipedia:

The UTR which occurs between the protein-coding genes contains the sequence for a ribosomal binding site (RBS) in the transcribed mRNA.  An RBS is a site where a ribosome can attach to the mRNA so that the Start codon of the following gene is in the correct position to begin translation of the protein.  (Of course, the 5' UTR preceding the first gene also has an RBS sequence.)  An RBS contains a particular nucleotide sequence to match up with a complementary sequence of the ribosomal RNA of the ribosome; this sequence is known as the Shine-Dalgarno sequence.

(Note that these inter-gene UTRs are not called introns; introns occur only in eukaryotes and occur within a gene, between the Start and Stop codons.)


If the body continuously produces new sperm, how is there room for it?

Your testes are a sort of waiting room where sperm hang out, and if ejaculation does not occur, they eventually die, just like red blood cells (or any of your body's cells). Once cells in your body die, they are broken down, and your body uses the components and nutrients to create new cells.

So it's a continual cycle of replacement and death.

Read more here


Does the use of UV light beam lead to poorer contrast in optical microscopy of cells than the higher wavelengths visible light?

Contrast in optical microscopy typically depends on different substances having different absorption spectra. Practically everything absorbs UV light, so there tends to be less contrast in that range than in the visible spectrum where there is a bit more selectivity.  All of this changes when there are contrast-enhancing substances added.  For example, molecules that absorb in one wavelength and emit at a different wavelength via fluorescence, attached to antibodies that bind selectively to specific cell components, can provide very high contrast.  E.g., see [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2156041/].

An alternative optical microscopy technique is phase-contrast microscopy which does not use absorption at all.  Instead, it measures the effective optical path length through the sample, which depends on local refractive index of the sample.

Yet another alternative is x-ray fluorescence microscopy, which can identify specific elements in the composition of a sample.  See, for example,[https://www.americanlaboratory.com/913-Technical-Articles/18833-Three-Dimensional-Elemental-Imaging-Using-a-Confocal-X-Ray-Fluorescence-Microscope/].


Many phenotypes might be normally distributed assuming a large enough population size and many QTL (Quantitative Trait Loci) as the normal distribution is a simple result of the CTL (Central Limit Theorem). If it is unclear to you, you should definitely have a look at the central limit theorem.

Typically, if the number of loci is too low, the phenotype may for example follow some kind of continuous approximation to a Poisson distribution. Of course, if the allelic effects are correlated among loci or if there is some linkage disequilibrium or if the phenotype is bounded or discrete, or nominal, you may not end up with a normal distribution of phenotypes but all of that is a discussion for another time.

  I can't come up with any obvious example of phenotypes that don't follow a normal distribution

As, the second quote says, think of any phenotype that is discrete. Here are a few examples

sex
right / left handed
eye color

Now if you want a quantitative phenotype that is not normally distributed, then height (which is the bad example of your first quote) is very slightly bimodal due to an average height difference between male and females (look at Are males taller than females in humans?). You can also think of any phenotypes that are bounded. For example running speed. Athletes will cause a very long right tail, while people in wheel chairs will make a big stack of probability mass in 0 km/h.

There is a lot of things to consider when trying to guess whether a is normally distributed or not in a population. It will take some good knowledge of statistics and good knowledge of the genetics of the population.


Do men have more extreme variations than women?

First of all for the first 22 chromosomes (and the mitochondrial chromsome) are the same between women and men. The X and the Y together are something like 1.5% of the total DNA in the human cell.  The X chromosome is also in common, so it has the same chromosomal (genetic) variations the same as women and men.

While I am not sure about the differences you point out, its for sure there are lots of differences between the biology of men and women!  The reason that women's traits might have different variances than men comes from the fact that in women there are 2 X chromosomes and in men there is only one, as well as the additional Y chromosome.

If there are any singular defects in the X chromosome a man carries, it will not be balanced out in the human male.  (other organisms have different sex chromosome schemes).  For instance because there is a cluster of genes that help the eye see in color, women's sense of color (i.e. from their cone cells) is sometimes better than men.  With 2 X chromosomes there is even the possibility of a woman who has four different color receptors in their cones.

On the other hand, why men see better in the dark (i.e. greater sensitivity in the rod cells), is possibly due to an extra Blue Rod pigment gene that remains on the Y chromosome (see above reference).  This is both an accident of genetics, but also an adaptive 'choice' that men would have different visual acuities than women.

Its also known that woman and men may have different epigenetic patterns, with some epigenetic modifications coming from the mother and others from the father.  This is adaptive and also not the direct result of the XY chromosomes.

Interestingly, it turns out that for the most part women's 2 X chromosomes are mosaic.  That is, in each cell only one of the randomly selected X chromosomes are active.  Recessive/dominant X genes are often not the case.

This could result in a greater observed genetic variance for women because when you have two chromosomes, often one of the genes is completely silenced.  Women display all of the alleles of their X chromsomes, whereas men have only one X chromosome entirely, the Y chromosome being much smaller.

So in other words, I would say that while men and women actually have the same variation in their DNA sequences, there are different patterns in the X and Y Chromosomes that might create more variance in terms of what we see in women's displayed genetic traits.


What is the difference between organelle membranes?

Great question. Turns out, there is some information about it.

For example, consider following resource: Membrane Protein Lipid Composition Atlas. Published by University of Michigan, it provides information on, primarily, protein content of different membranes from different species, but also has a list of lipid content.

Just as an example, consider following difference between membranes of mitochondria in yeast:

Now, concerning your interest in biophysics. To my taste, starting with just bulk lipid composition is a good first approximation. Although you also want to know about lipid raft formation and density/distribution of proteins. Next step, probably, will be symmetry considerations, that is, difference between sides of same membrane. You can imagine membranes with same bulk composition, but because of different lipid position (in/out) properties will be different.

It seems you can assess raft composition based on membrane lipid composition. Membrane capacity also is a property of membrane content.

Following quick walk through this Google Scholar search provides even more links between biophysical properties and lipid bilayer composition. However, it might be challenging to find exactly what you are looking for.


Is it possible to live without health problems sleeping one day and not the other?

I'm not aware of any study testing this hypothesis. I would surmise that adverse health effects are likely because the circadian clock operates on a 24-hour time frame, and because lack of sleep for ~40 hours every second day will alter hormone, cytokine and other measures to levels not normally seen in 8-hour sleep/16-hour wake cycle.


It's a pellucid fly, a species of hover fly. scientific name: Volucella pellucens
https://www.naturespot.org.uk/species/pellucid-fly


What Websites Have Image Libraries for Bacteria and other Microorganisms

While I doubt that this might be possible in all cases (and I would be careful about classifications), there are indeed some great ressources, which contain a lot of images. Since there is a vast number of bacteria present on this planet, there is of course a limitation to bacteria available in photos, representing only the most common or important.

These are:

Bacteria in Photos
American Society of Microbiologies Microbelibrary
Microbiology in Photos

Then there is an information page available from the CDC, which informs about parasitic diseases. These are non-bacterial, but probably also interesting. It can be found here:

Laboratory Identification of Parasitic Diseases of Public Health
Concern


Why do orcas eat only the tongue of whales, liver of sharks, etc.?

Killer whales have a wide range of prey. They hunt in coordinated packs called pods. They are very organized on a hunt and each has a specific job prior to the kill.

Where the confusion might be coming from is that different pods have different habits. It is true that Orca's have been witnessed eating only the tongue, this is not the norm. They tend to eat the tongue first because it's muscle, with lots of protein. Plus, they like the tongue, as we like a good steak. However, in most cases they will consume as much of a whale (typically baleen, or blue whales) as they desire. In fact, whalers hate them because they will follow whaling ships and wait for the fishermen to harvest a whale. They will then rush in and gorge themselves. Another case of them only eating the tongue is when they are well fed. In this case, they can afford to be picky and may only eat the tongue. Oh, by the way, the average tongue is the size of an elephant. So, it's no small meal.

As for sharks, it's pretty much the same scenario, however, there are many cases of Orca's only eating a great while shark's liver. The reason they target the liver (and they do it with surgical precision) is because it contains large amounts of a compound called squalene. Squalene is important to synthesis of certain chemicals in the Orca's body. They will also target the heart, as well. The attacks of great white's is a more recent trend among killer whale pods. They are quick learners and once they feel the benefits of these organs, they will then focus on the sharks when their bodies tell them they need the squalene. Of course, they don't know that. They just know they feel better and stronger after consuming GWS organs.

There may be pods out there that tend to have these habits (outlined above) more than others. Resident pods (staying in one area) seem to be calmer and are not as likely to have the tongue activity, but it is the residents that are often that which kill the GWS's for their organs.

Transients are far more aggressive than residents. They are likened to pack wolves and will do some extremely cruel things (by human standards). These are the one who are far more likely to eat only the tongue of a whale. It could be that since the shark organ habit hasn't been happening for very long, it's the residents who figured out the connection between health and these shark organs.

Another factor that could come into play is that scientists/marine biologists tend to believe that there are different species of killer whales. This may play a role in dietary habits as well.

Killer whales are the top (known) predator in the water. While a much larger whale, or GWS could potentially kill one, they are typically no match for a pod and will instead steer clear and only fight if no other alternative presents itself.

I hope this helps. I'm no expert, I've just done my research.


'Pore' is a confusing term. Sweat is produced in sweat glands, and subsequently excreted through a duct, as indicated in the image below (sudoriferous ~).

In short, viruses cannot enter the body through these glands because the glands don't really open up into the body, but instead the inside of the sweat gland is lined with sweat-producing cells (fig 2 and 3).

A passive protection mechanism preventing infection is similar to the mechanism by which the bladder is guarded from infection through the urethra: even if some malignant agent were to enter the sweat duct, it is simply pushed out by the excreted sweat.

Figure one: Sweat glands in skin. Source: wikimedia commons.

(source: uwa.edu.au)

Figure two: Slide of sweat gland. Tightly packed secretory cells dump sweat into the lumen through exocytosis (see fig 3). Source: University of Western Australia.

Figure three: Exocytosis. The lining of the sweat gland contains cells producing sweat through exocytosis. Viruses and other pathogens cannot simply enter these cells, and also cannot 'slip in between' the cells. Source: wikimedia commons.


I am not an ornithologist, but using identify.whatbird.com and a simple google search, this appears to be a Muscovy Duck. Try a google image search for yourself! Some of the birds pictured have more ostentatiously red or larger caruncles, but some look very similar to the birds you photographed. For example: http://www.birdinginformation.com/birds/ducks/muskovy-duck/

From muscovyduckcentral.com and identify.whatbird.com:
The domestic breeds can come in a variety of colors, but are primarily black and white with red and white bills. The males are larger than the females -- around 15 lbs for a male and only 8 lbs for a female. Females are duller colored than the males. Muscovy ducks are indigenous to Mexico, Central and South America, but are now raised in many different locations. They are considered a good duck stock because they are large, breed quickly, provide good pest control, and are quieter than many other duck breeds.


Can a woman give birth to twins with different fathers?

Yes, this is possible through something called heteropaternal superfecundation (see below for further explanation).

Of all twin births, 30% are identical and 70% are non-identical (fraternal) twins.

Identical twins result when a zygote (one egg, or ovum, fertilized by one sperm) splits at an early stage to become twins. Because the genetic material is essentially the same, they resemble each other closely.

Typically during ovulation only one ovum is released to be fertilized by one sperm. However, sometimes a woman's ovaries release two ova. Each must be fertilized by a separate sperm cell. If she has intercourse with two different men, the two ova can be fertilized by sperm from different sexual partners. The term for this event is heteropaternal superfecundation (HS): twins who have the same mother, but two different fathers.

This has been proven in paternity suits (in which there will be a bias selecting for possible infidelity) involving fraternal twins, where genetic testing must be done on each child. The frequency of heteropaternal superfecundation in this group was found (in one study) to be 2.4%. As the study's authors state, "Inferences about the frequency of HS in other populations should be drawn with caution."


By what mechanism can hypoglycemia induce fainting?

There are regulatory mechanisms that may prevent moderate hypoglycemia to progress to a more severe state, however these mechanisms act before lack of conciousness sets in. The progression of hypoglycemia may depend on overall health and medical status and vary between healthy and diabetic persons, for example.

Rosenthal et al. (1) write that

  The brain is normally dependent on glucose for oxidative metabolism
  and function. Acute iatrogenic hypoglycemia, occurring as a result of
  insulin excess during the treatment of type 1 diabetes, can cause
  clinically significant cognitive impairment. In health, such
  hypoglycemic cognitive dysfunction does not occur. Endogenous
  counterregulatory mechanisms are activated in response to a small
  reduction in circulating glucose, preventing more profound
  hypoglycemia. In diabetes, the inability to reduce circulating insulin
  levels (1), the failure of glucagon responses (2), sometimes
  accompanied by defective autonomic and adrenergic responses (3), can
  allow plasma glucose levels to fall low enough to result in detectable
  disturbance of cognitive function, ranging from a subtle slowing of
  reaction times (3) to coma (4).

In short, the brain malfunctions due to lack of glucose (the sole energy source for the brain). Note that cognitive impairment and unconciousness can also occur in otherwise healthy persons, for example in the case of prolonged exercise combined with lack of nutrition. The exact cause of cortical dysfunction is not known:

  Impairment of brain function is a recognized consequence of acute
  hypoglycemia. It is known that different brain functions have
  different susceptibilities to acute hypoglycemia; for example, the
  triggering of autonomic activation, a hypothalamic function, occurs in
  response to quite modest decrements in circulating glucose
  concentrations (5,6,7), whereas significant cortical dysfunction
  requires more profound glucose deprivation (3). Even within different
  cortical functions, there is variation in hypoglycemia susceptibility
  (26). The mechanisms of cortical dysfunction during hypoglycemia are
  not known.


Are restriction enzymes active at −20 °C?

Enzymes have temperature optima based on the organism they were isolated from. So I would predict the there is virtually no activity at −20 °C. Another consideration is that the reactions are likely to be frozen solid, so that would limit diffusion, and also slow it down. But the real question is: what are you afraid of? Just the star activity? Even if there were star activity, would that adversely affect your experiments?


What determines if a small protein / large peptide is immunogenic?

Edited to delete off-topic section:

Most (all?) proteins are ultimately immunogenic. You can't really design your way around immunogenicity, which is a good thing, because otherwise we'd all be dead from viruses.

Obviously not all proteins are equally immunogenic, but basically all protein therapeutics are immunogenic at some rate. One thing that seems positively associated with immunogenicity in that review is quaternary structure, but it's quantitative not qualitative.

Some of the commonly used synthetic antigens used in biochemistry such as HA C-terminus (24 residue) or FLAG (8 residue) are quite small.

More generally, this study finds that even 3-5 residue peptides can be sufficient to raise immune responses. So likely any polypeptide is potentially immunogenic.

Such small peptides are unlikely to have meaningful secondary/tertiary structure. My guess is that that you would have to have a pretty structurally strange protein to avoid any potential immune response. However if you had an insoluble or somehow sequestered protein you might be able to avoid it, but I'm not an expert so I can't say how.


If targeting a certain daily water intake, do you have to compensate for beverages that promote diuresis?

The notion that tea and coffee are diuretic and don't count in your daily waterbalance, is an urban myth. At most, both are mildly diuretic (if any).

The assumption is based from an old study from 1928 with only three participants. While the small number of participants alone is a good reason to reject the study (it would never get published today) because the findings would lack any statistical power, the design is also questionable. You can find this story in reference 1 if you want to read it.

It is known that large amounts of caffeine indeed have a diuretic effect by increasing the blood flow to the kidneys and inhibiting the reabsorption of sodium. This leads to the outflow of water and an increased production of urine. See reference 2.

However, reference 3 found that this diuretic effect (which is only present at high concentrations of caffeine) diminishes due to tolerance when people regulary drink tea or coffee. They do not see any diuretic effect from normal tea, coffee or caffeinated beverages.

The explanation for this effect is most likely a misinterpretation of our observation. We seem to produce more urine when we drank tea or coffee, but we wrongly compare it to a time when we drunk nothing. If we would compare it with a time, when we drank the same amount of water, the effect (you have to pee more when you drank something) would be the same.

Drinking tea and coffee will therefore help to keep our waterbalance, as would water, juice or softdrinks.

References:

TOLERANCE AND CROSS-TOLERANCE IN THE HUMAN SUBJECT TO THE DIURETIC
EFFECT OF CAFFEINE, THEOBROMINE AND THEOPHYLLINE
Caffeine and the Kidney: What Evidence Right Now?
Caffeine ingestion and fluid balance: a review.


Purportedly White House Spokesman Sean Spicer consumes (chews and swallows) at least 35 pieces of gum every day.

Mastication breaks down the components and carbs, oils and alcohols are digested accordingly, but the rubber is pushed through by your intestinal muscles. You might enjoy this article which goes into detail about the breakdown and digestion of "gum" constituents. For the most part tho the rubber in gum passes through like corn, peanuts and such.

So, no - no "seven years" to digest. I remember hearing that as a kid. I think it is the kind of thing kids are told to discourage them from swallowing outright instead of chewing gum.


Can someone help me identify this Brazilian spider?

Interesting!  See those long spines on the legs?  Only two groups of spiders (that come to mind, anyway) have that sort of arrangement:
Lynx Spiders (Family Oxyopidae) and Pirate Spiders (Family Mimetidae).
Lynx Spiders are wandering hunters, and the ones I'm familiar with tend to have a body shape more like the familiar Grass Spiders (longish, tear-drop shaped abdomen and hunters cephalothorax - roughly rectangular, and often very blocky at the face.
For instance:
https://bugguide.net/node/view/1965

https://bugguide.net/node/view/1489229/bgimage

So, your spider looks to be a South American Lynx Spider, which unfortunately I'm not at all knowledgeable about.

I'm going to discount Pirate Spiders as a possibility, even with the association there with a bit of web (Pirate Spiders invade other species' webs and kill the occupants), because they're much more 'orb-weaver'-like in their general body shape.  This one is so Lynx Spider-like that I am pretty confident that it is one of those.


Like in the blood, intracellular lipid trafficking is facilitated by vesicular transport and lipid carriers like fatty acid binding proteins. In addition, intracellular membranes are densely packed and they can exchange lipids by collision and transient hemifusion. If you have access to Cell, a good review is from Prinz W. 2010 Lipid Trafficking sans vesicles, Where, Why, How?


How are the dominance and additive effects reflected in the mean and variance of the offsprings of two individuals with known phenotype?

What is the expected phenotypic trait of an offspring given the phenotypic trait of its parents?

The expected trait of the offspring is equal to the mean of the parents traits.

For this I assumed we don't have more information about the genetic of the trait (typically, without knowing the directionality of dominance and number).

  What is the expected phenotypic trait of the offspring population given the phenotypic trait of the parent population?

As a consequence of the above, the expected mean phenotypic trait of the offspring population is equal to the mean of the parent population (in absence of selection).

  What is the expected variance in the offspring population?

No drift, no selection

In absence of drift and selection (and environmental changes), the variance of the offspring population equals the variance of the parent population.

Directional selection only

In presence of directional selection, please have a look at How does Natural Selection shape Genetic Variation? and ask follow-up question if needed.

Drift only

In presence of drift only, the heterozygosity is reduced by a factor $\frac{1}{2N}$, where $N$ is the population size. The loss of genetic variance is then dependent on (1) the frequency, (2) the dominance and (3) the effect size of alleles at loci causing this genetic variance. There is therefore no simple answer. The only generalization that can be done is that (1) the expected variance of the offspring population is lower than the variance of the parent population and (2) the smaller the population size, the higher is the expected loss of genetic variance

General Note

My feeling about quantitative genetics (but I am not really an expert in that field) is that it is often frustrating to see that generalization is often impossible and general solution to recursive equations often don't exist implying that predictions to more than one generation must be calculated through iteration.

I suspect that an expert in quantitative genetics would be able to say much more than me in this post.

The book Introduction to Quantitative Genetics (by Falconer and Mackay) is probably still the best book to increase your knowledge in quantitative genetics.


Organ cloning - possible to make a non-antigenic organ?

I'll contradict the answer posted here (ages ago) and say no, it isn't possible. Growing an organ wthout MHC proteins might be achievable, but it would be rejected for not having MHC1. NK cells instruct all cells without MHC1 to perform apoptosis. In this case, MHC1 antigens are required on cells for proper self-identification.

Keeping MHC1-less cells alive could be achieved by

equipping them with whatever is keeping erythrocytes and thrombocytes (also lacking MHC1) from being destroyed on sight. (A good idea, but see next paragraph)
disabling their apoptosis mechanism (Cells with disabled apoptosis mechanisms are commonly referred to as cancer, so we might want to not do this.)

MHC1 also has a function; it presents "peptide shreddings" from proteosomes to T cells; this way T cells can check if the cell contains internal foreign proteins (sign of a virus infection or cancerous transformation). Thus, removing MHC from the cells would make them very liable to become nearly unstoppable virus factories or tumor cells.

(On a side note, while everyone technically can receive 0 Rh negative blood, group-identical blood is used always, except in rare emergency cases. A and B antigens here, as far as I know, do not have function.)


Is it possible to add a new sequence to a blast database without recreating it from scratch?

You can use blastdbcmd to extract FASTA sequences from the BLAST database. Then you can append your extra sequence to the newly created FASTA file, and remake the BLAST DB using makeblastdb. Assuming you have a protein BLAST database in the current working directory, and a sequence you want to add to it in new.fa:

$ blastdbcmd -db proteindb -dbtype prot -out db.fa -entry all
    $ cat new.fa >> db.fa
$ makeblastdb -in db.fa -out newproteindb -dbtype prot

(Replace prot with nucl if you have a nucleotide database)


Nerves, Neurons, Axons and Dendrites by Example

Receptors are typically not located in a neuron. Instead, receptors generally synapse onto a primary neuron, and specifically on the primary neuron's dendrite;
Within the neuron physiological signals are received in the dendrite and are transmitted uni-directionally via the axon to the axon terminal. Between neurons the signal is transmitted from axon to dendrite via the synapse (see figure).
Although axo-axonal communication exists, it is not the typical way of neural communication (they are regulatory in nature and do not convey information as such). Typically, axons synapse onto another neuron via the dendrite of that second neuron.

The typical connection is the following:

Nerves typically do not contain cell bodies, only the elongated parts of neurons, i.e. the axons. A nerve is a bundle of axons that contain closely related signals from closely related structures in the body.


What is the scientific name of this evergreen plant?

The tree in question belongs to the Araucariaceae family,

There are multiple species of Genus Araucaria,

I'd place Araucaria araucana on the first place, but there are multiple others:

Araucaria araucana

Araucaria luxurians

Araucaria columnaris

Araucaria subulata


Data for giraffe subspecies population change over the time.

In a recent paper in Current Biology, Fennessy and colleagues conclude that there are four species of giraffe and that their numbers are declining in Africa. Giraffes (Giraffa camelopardalis) are presently classified as one species, with nine subspecies, which are considered ‘Vulnerable’ on the IUCN Red List. The present consensus of one species divided into nine subspecies has previously been questioned (Supplemental information), and Fennessy and colleagues provide another viewpoint on giraffe taxonomy. The fundamental reason for different taxonomic interpretations is that they are based upon different datasets that adopt different statistical techniques and follow different criteria for nomenclature.
Its basically a form of evolutionary process.
Living giraffes were originally classified as one species by Carl Linnaeus in 1758. He gave it the binomial name Cervus camelopardalis. Morten Thrane Brünnich classified the genus Giraffa in 1772. The species name camelopardalis is from Latin.
The giraffe is one of only two living genera of the family Giraffidae in the order Artiodactyla, the other being the okapi. The family was once much more extensive, with over 10 fossil genera described. Their closest known relatives are the extinct deer-like climacocerids. They, together with the family Antilocapridae (whose only extant species is the pronghorn), belong to the superfamily Giraffoidea. These animals may have evolved from the extinct family Palaeomerycidae which might also have been the ancestor of deer.
The elongation of the neck appears to have started early in the giraffe lineage. Comparisons between giraffes and their ancient relatives suggest that vertebrae close to the skull lengthened earlier, followed by lengthening of vertebrae further down.One early giraffid ancestor was Canthumeryx which has been dated variously to have lived 25–20 million years ago (mya), 17–15 mya or 18–14.3 mya and whose deposits have been found in Libya. This animal was medium-sized, slender and antelope-like. Giraffokeryx appeared 15 mya in the Indian subcontinent and resembled an okapi or a small giraffe, and had a longer neck and similar ossicones. Giraffokeryx may have shared a clade with more massively built giraffids like Sivatherium and Bramatherium.
Further on researches are also being made till now!


A colony of humans are sent to an alien world, at what point would the descendants evolve to be genetically incompatible with Earth humans?

That's an interesting model, because mosquitoes are vectors for serious illnesses, so are pretty well studied.  One team of scientists are working on genetically altering mosquitoes in Africa to make them unable to transmit the parasite that causes malaria. As the mosquitoes breed, it spreads through the population. In an interview, the lead researcher stated:

  In the lab, we saw the mutation spread to more than half the population of mosquitoes we had living in cages. This happened in a time span of 12 to 16 generations of mosquitoes (each generation being between 18 to 30 days in the wild). So it's quite efficient.

12 to 16 generations for one mutation to spread to half of a contained population. In human generations, 16 = 320 years, and that doesn't take into account fertility rates, miscarriages, etc. (Not a problem for mosquitoes, I presume).

How many mutations would it take to make two humans incapable of reproducing without endangering their own health or fertility? Excluding all of the harmful mutations that might just result in disease or decreased fertility? And add to that that the males need to change as well as the females? No one knows.

Imagine a cystic-fibrosis type mutation (one gene) that increased the viscosity of cervical mucus such that normal sperm could not fertilize the egg. There would need to be another mutation in males that would make sperm stronger, or secrete an enzyme that breaks down mucus, or something to that effect. However, look at Cystic Fibrosis. People used to die before adulthood. Most men with CF are sterile. Women with CF, living longer now because of better care and treatment, are getting pregnant, but many have a decreased lifespan post-pregnancy, and almost all the babies are premature. You can't predict "when" a series of beneficial mutations so dramatic as to change a being so dramatically. The answer might be never.

Try to give me a single or a few mutations that would prevent the ability of people from one population and another to mate. Say one mutation led to a smaller pelvis. Most women with that mutation would die in childbirth before a mutation arose to make smaller babies (which would most likely be a deleterious mutation as well).

I am not a geneticist (which is really the person who should be answering this question) but I think the odds of this scenario ever occurring are very low. I just can't imagine mutations making reproduction impossible between two populations being beneficial and selected in one population rather than harmful. Keep in mind that different humans from populations that were isolated for many thousands of years have no problem reproducing.


1)
You know most bridges have vertical cylindrical pillars.

This is probably because cylinder is among the strongest 3D structures to support anything.
So, cylindrical trunk provide best support for tree crown.

2) Most accurate
It is natural for any cell to grow equally in all directions. This, leads cells to expand in all directions equally in a circular girth.

3)
Resistance
Cylindrical girth provides least resistance to air. So, tree naturally takes this shape to prevent damage by air strikes.

4) Read
 https://m.reddit.com/r/askscience/comments/1973mh/

for more info.

5) http://www.stevespanglerscience.com/lab/experiments/balancing-act-cylinder-strength/

for strength of Cylinders.


Energy use by muscles, actual work done by muscles and more

I speak only for the U.S. regulations: the calorie labels on wrappers refer to the energy released when burned. Sometimes these are inaccurate. Many dieticians recommend calculating the calories based on weights of protein, carbohydrates and fats in the serving: 4 kcal in each gram of protein and carbohydrate and 9 kcal in each gram of fat in your food. Multiply carbs, proteins and fats by the appropriate value and add them up.
The reading on the bike does not take into account your pulse. Just the raw work done turning the pedals. Some very smart bikes do take pulse into account, but the often inaccurate heart monitors lead to inaccurate calculations of total energy.
The heart and diaphragm (muscle primarily responsible for breathing) do use more energy when exercising than when you are sitting still. But that increase is small relative to the increase in the primary muscle sets involved in the exercise. Your resting heart rate is probably around 70 bpm, your exercising heart rate is probably around 160-180 bpm. So it has increased its rate and energy consumption by about 3 times. Your skeletal muscles maintain a basal metabolic rate during inactivity (one purpose of this is your body needs the heat from slightly tensed muscles to thermoregulate itself) - but during exertion, their metabolic rate increases enormously. Exercise increases their energetic demands by whole orders of magnitude.

The actual value of the (energy used by heart) / (energy used by skeletal muscles during exercise) depends on what exercise you do and how efficiently you do it. The change in the ratio between inactivity and activity depends on how much muscle mass you have (more muscle uses more energy during inactivity) and how strenuously you exercise. But the point is that the increased energetic demands by skeletal muscles far outpace the 3x increase in energetic demands by the heart and diaphragm - so the latter accounts for pretty much all total energy consumption at even moderate activity levels.


I didn't watch the video so I don't know if this was mentioned. Butterflies will exhibit a behavior called mud puddling which occurs mainly with male butterflies [1]. Puddling is when butterflies seek out moist surfaces in order to consume the fluid. Butterflies will puddle in soil, dung, carrion (rotting flesh/meat), etc. Boggs and Jackson claim that puddling falls into two categories which aren't mutually exclusive [1]:

scarce nutrients for example sodium
competitive exclusion of males or young individuals from flowers

But we can see blood isn't the only option for puddling. Basically anything that provides moisture and nutrients will do.


Do Black Pepper and Black Nightshade share specific characteristics?

Short answer
Nigrum is Latin for 'black'. As you write in your post, it's black pepper and black nightshade. Not until the level of Class and Phylum do they share the same taxonomic classification. Hence, the species suffix nigrum doesn't tell you anything about their kinships, other than their physical appearance (they're both black).

Background
In general, the species part of the linnaeus nomenclature has nothing to do with evolutionary relationships. Instead, it is the higher classifications that denote kinships, for example, as you already suggest, the genus name, that may have various related species in it (Fig. 1). The species you mention are of a different genus.

The Species: Piper nigrum belongs to the Genus Piper, Family: Piperaceae, Order: Piperales, Class: Magnoliopsida, Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya
The Species Solanum niger belongs to the Genus Solanum, Family: Solanaceae, Order: Solanales, Class: Magnoliopsida (Dicotyledons), Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya.

They share only the same Class (and hence Phylum, Kingdom, Domain). For comparison, in the Kingdom of Animalia, we have the Phylum Chordata (vertebrates), that splits up into the Classes Mammalia (Mammals), Actinopterygii (Bony Fish), Chondrichthyes (Cartilaginous Fish), Aves (Birds), Amphibia (Amphibians) and Reptilia (Reptiles). So your two plant species share as much in common at the taxonomical level, as Mammals and bony fish.

Piper nigrum (or black pepper), is a climbing vine in the Piperaceae (pepper family) native to the Malabar region of southwestern India. Black pepper is grown in various tropical regions, including India, Indonesia, and Brazil, as it is one of the most important spices in the world.

Solanum nigrum (or European black nightshade) is a species in the Solanum genus, native to Eurasia and introduced in the Americas, Australasia, and South Africa. It is also known as black nightshade, duscle, garden nightshade, Indian nightshade, garden huckleberry, hound's berry, petty morel, wonder berry, small-fruited black nightshade, or popolo.

Fig. 1. Linnaeus nomenclature


Why is Ibuprofen contraindicated in asthma patients?

Ibuprofen is an NSAID. So it acts by inhibiting COX (Cyclooxygenase) enzyme. What it signifies is that, if COX enzyme has been blocked, the PUFA (say arachidonic acid, here) will be converted to leukotrienes through lipoxygenase pathway.

Leukotrienes (LT) are of different types and have several target receptors; one of which is CysLT-receptors on bronchial smooth muscle. Once they are activated through LTD$_4$,E$_4$,C$_4$ , bronchospasm will occur. For asthma patients this is really fatal. So for them Ibuprofen is contraindicated.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5072955/
Lo, P.C., Tsai, Y.T., Lin, S.K. and Lai, J.N., 2016. Risk of asthma exacerbation associated with nonsteroidal anti-inflammatory drugs in childhood asthma: a nationwide population-based cohort study in Taiwan. Medicine, 95(41).


From the Biology Online Dictionary, refractile refers to:

  ... the ability of cellular granules to refract or scatter light.

Tumor cells can be more "dense", as they are usually rapidly dividing, and so need extra ribosomes to maintain protein production, may have a higher DNA/RNA content reflecting increased transcription and duplication, more mitochondria to power the cells, etc. This can alter the refractive index of a suspension of tumor cells as compared to organ-matched normal cells, for example.


The optic nerve fibers cross inside the optic chiasm sharing the same shell:

The crossing fibers go ones between others, like on this classical picture -


Are we "more evolved" than present-day bacteria?

This is a standard question. The whole problem boils down to what you mean by "more evolved"? Below I am answering the question considering a number of possible definitions. If you have other ("clearly defined") definitions in mind, let us know.

  Are [humans] "more evolved" than present-day bacteria?

If "more evolved" == "more evolution time"

Then, both bacteria and humans are exactly as evolved!

As all life on earth shares a common ancestor, all currently living creature has evolved for exactly the same amount of time (about 3.8 billion years).

If "more evolved" == "more generations"

Then, bacteria are more evolved.

Bacteria typically have a much shorter generation time than humans do, so with this metric, bacteria would be more evolved.

If "more evolved" == "more fixed mutations since the MRCA"

Then, it is a little more complicated and may depend upon which bacteria lineage you are considering.

If the genome-wide mutation rate is $\mu$ and the haploid population size is $N$, then there are $N\mu$ new mutations every generation. Given that each one of these mutations has a probability of fixing (fixing = reaching a frequency of 1 in the population) is $\frac{1}{N}$, the rate at which mutations fix is $\mu N \frac{1}{N} = \mu$ at each generation. If a species has $g$ generations per year, then over $t$ years, $\mu g t$ mutations would have accumulated.

The genome of bacteria is typically much smaller than the one of humans, but their mutation rate per nucleotide is much higher. Overall, the genome-wide mutation rate is rather higher in humans but that might well differ from species to species. However, again, bacteria have had more generations per year than humans and therefore bacteria species likely have fixed more mutations than humans have. So from this metric, bacteria are rather more evolved than humans.

If "more evolved" == "able to resist higher acceleration"

Then, bacteria are more evolved although that might among bacteria lineages

Some bacteria have been grown under 400,000 g (National Geographic), while a typical human can only tolerate about 5 g and for only a short period of time!

If "more evolved == more impact on the environment"

The term impact is a little hard to define but I think it is of interest to highlight that, even here, bacteria would probably win because cyanobacteria caused the great oxygenation event which is probably the largest planet-wide environmental change caused by biological organisms.

(thanks @Thawn for this definition he gave in the comments)

If "more evolved" == "having more lungs"

Then, humans are more evolved.

Bacteria have no lungs, humans have two.

If "more evolved" == "bigger genomes"

Then, humans are more evolved. Note also that corn would be more evolved than humans with this metric!

If "more evolved" == "higher fraction of the genome that is encoding for proteins"

Then, bacteria are more evolved.

If "more evolved" == "more protein coding sequences"

Then, humans are more evolved.

If "more evolved" == "more phenotypically different from the MRCA"

You would have to list specific phenotypes of interest. So, here the term "more evolved" still remained a little undefined.

Also, we do not have much information about the MRCA of these two highly distantly related lineages. The question could be more easily answered for more closely related lineages. For example, in mammals, if you consider the following traits and always ask what species is (likely) most different from the MRCA of all mammals

body mass -> blue whale
brain mass -> sperm whale (yes, sperm whales have a very big brain)
lips shape -> platypus (they have a beak)
time taken to type Hello\nWorld on a computer keyboard -> humans

Related posts

What is meant in biology by the term “evolved”?
Why have humans evolved much more quickly than other animals?


What tests can be performed to test the purity and quality of the raw peptide HCG (Human Chorionic Gonadotropin)

A monograph from a pharmacopeia gives a good starting point for active pharmaceutical ingredient characterization. AFAIK there is no monograph for hCG nor your actual peptide of interest, but there is one for FSH (here for the european pharmacopeia monograph), which shares a subunit with CGA, meaning that modifications of it could suffice (though validating these modification will be a good amount of work, and will depend on the ultimate use for the peptide).
First, it is necessary to stress that even if the compound passes all assays, it would still be unsuitable for human use. It may be acceptable for animal experimentation. This is because the pharmacopoeia assumes a context where you have a non-adversarial relationship with your supplier, such that statement like "up to XX% remaining impurities" is an acceptable standard as the synthesis route & typical impurities are known. However, buying peptides from a random Chinese seller with no transparency on process is likely an adversarial situation.
Some keys to read the monograph:

Compound followed by the letter R ("water R", "glycine R"): these compounds have their own monograph. You could assay them accordingly, but for this use case understanding the R as "analytical grade" is possibly good enough.
"Follitropin CRS": chemical reference substance, a reference standard powder of follitropin obtained through reliable means (typically through EDQM for pharmaceutical purpose). Here also, substituting for an analytical grade standard from a reputable chemical seller could work.
Method followed with three numbers ("Bacterial endotoxins (2.6.14)"): reference a method monograph found in the given chapter/section. Apply methodology as described in the referenced text.

To adapt the assays to your peptide of interest, you need to understand which parts are specific to follitropin (and should be modified), and which applied to gonadotrophin-like peptides in general. For instance, for isoelectric focusing, the running conditions (pH, catholyte/anolyte) will be adequate, but the follitropin reference will be replaced with a CGA reference. On the contrary, the selective cleavage of peptide bonds assays is specific to the peptide, and will need extensive rework.