Can a carnivorous animal consume plants with no adverse effects?

This is kind of a weird/trick question.  How long do you want the animal to live?  If the lifespan is shortened or compromised does that fit....   Obligate carnivores (cats, dogs) do eat plant material.  In the wild cats mainly eat grass to get rid of hairballs.  Cats are more impacted by phytotoxins than dogs.  However, both, are extremely vulnerable to compounds that don't bother humans (xanthines like theobromine, caffine, compounds in garlic, onions, broccoli, mushrooms).  Cats can't convert plant fats into what they need (we can) as a result they can go blind if they don't get the animal fats they need.  Likewise, herbivores will suffer increased cancer, heart disease, renal failure from diets with animal fats / protein.  Your mention of "wolf" is interesting because there is a South American wolf that supplements its diet with a tomato relative (called something like "fruit for wolves" in Spanish).  This is probably only "good" for it in that it keeps the wolf from otherwise starving.  I don't know that it has a strong deleterious effect (probably not, but it could be more sensitive to trace alkaloids in the fruit) but it could hurt it in a minor way.


What is immunosuppression? Why would one use it?

Immunosuppression is not used in cancer, in fact it is typically harmful unless of course the cancer is a immune or white blood cell cancer where suppressing their growth may be helpful. What you are perhaps alluding to is that an adverse effect of cytotoxic chemotherapy used in the medical treatment of cancer can cause immunosuppression.

Immunosuppression is helpful when it is causing more harm than good. The immune system is powerful and sometimes when its fighting an infection it can go a little overboard and cause enough damage to harm someone in the long term. In this case immunosuppression is helpful in preventing too high a response. For example in an organ transplant the recipient's immune system may destroy the new organ, but immunosuppression can prevent rejection.

Another case is when there is an autoimmune or inflammatory condition occurring. Rheumatoid arthritis being an example of the former and asthma being an example of the latter. In these diseases inflammation due to the immune system perhaps targeting our own body cells causes damage to our organs or cells and causes the disease. Immunosuppression here can limit or prevent further degradation or sometimes even reverse damage due to inappropriate immune responses.

Interestingly the human body must keep a good balance between being under and overactive. Certain individuals with better ability to control HIV infections or other infections are genetically more likely to also get autoimmune conditions.


A motif is a pattern that you discover in a structure by analysis. For example, common sequence motifs are short sequence fragments with parts similar to a regular expression. So, if you have a motif like "A*C" this matches to the sequences "AAC" and "ACC" but not to "ACA". You can reverse the process to discover the motif from the sequences.

Similarly with structural motifs in proteins. A beta-hairpin is :

  The motif consists of two strands that are adjacent in primary
  structure, oriented in an antiparallel direction ... and linked by a
  short loop of two to five amino acids.

So first you have to determine where the strands and loops are, then how the strands are connected into sheets, and finally recognise the hairpins. It is the definition of the motif itself that determines how you discover it.

Some resources that might be helpful are:

Motivated proteins (Small h-bonded motifs)
The protein topology graph library (Larger motifs)
The protein geometry database (Not really motifs, but interesting)
PDBeMotif (define and search for motifs in the PDB)


What makes some viruses more infectious than others?

To name a few parameters that can determine the infectiousness of a pathogen:

Transmission pathways used (aerosols, surfaces, vector organisms, feces etc.)
Molecular affinity to bind to host cell (how well does it penetrate the cell)
Strategy within host cell (lysogeny, lysis)
Interaction with the host’s immune system


"Frank dehydration" is not really a regular medical term. You can suspect this by using Google search with "frank dehydration" in quotes and site:gov (only 3 websites showing up) and site:edu (2 websites) operators.

The term "frank dehydration" as an informal term can refer to "obvious," "actual," "test-confirmed" dehydration as opposed to feeling dehydrated or thirsty.

Tests to confirm dehydration include a combination of the body exam (dry mouth, prolonged skin turgor, decreased body weight), urine tests (dark urine, increased urine specific gravity, decreased urination frequency and 24-hour urine volume) and blood tests (increased sodium levels - hypernatremia).


I don't think so naturally. I think the general stream of the progeny goes stem cell => pluripotent cell => progenitor cell => specialised cell.


I know this question is a bit old, but I read a paper recently which (claimed) to answer this question.
I think the answer to this question is suprisingly controversial. I don't really have a formed opinion yet of which answer is correct, but I will try to discuss the different viewpoints here.
Argument 1: Sweeps are rare
On one hand, we have the people who are sceptical of how common sweeps are. This, in my understanding is most researchers. Many people believe that polygenic is the predominant form of selection in humans.
There is the paper by Hernandez et al (2011), who find scant evidence of selective sweeps in recent human history. Essentially, they looked at the reduction in diversity (something which is associated with sweeps) around amino acid substitutions and synonymous substitutions and found that the two were statistically the same. They say it's probably more likely that this is caused by strong purifying selection at linked sites rather than sweeps.
Szpak et al (2019) suggested that most of the time, the criteria for designating something a sweep in human populations was probably too lax, and many of the previouly claimed sweeps were probably artefacts of some kind. In fact, they only find compelling evidence for 2 sweeps in recent human history.
Argument 2: Sweeps are more common
Alternatively, there are some studies which have apparently discovered a relative abundance of sweeps in human history. Some might make the argument that sweeps are likely to be common, since humans have a relatively small effective population size (~20,000) and low mutation rate.
Souilmi et al (2020) claimed to have discovered 57 (fpr<10%) sweeps using genomes from ancient Eurasian individuals. 35 of these 57 were inferred to have occured before 35kya. The reason they claim to have found many more sweeps than previous studies is because they used ancient DNA. It is well established (Hellenthal et al 2014) that admixture is virtually ubiquitous within modern and ancient human populations. Admixture likely obscures the signal of sweeps by introducing non-selected haplotypes from the admixing population, making hard sweeps look like soft sweeps, or perhaps not even sweeps at all. They confirm this using simulations and show the power to detect sweeps is massively reduced when you are looking at admixed populations.
However, their method uses ancient DNA, which is highly prone to various artefacts, which they didn't appropriately test with simulations. It also hasn't been peer reviewed, so there may well be other potential issues.
References
Hernandez et al 2011
Szpak et al 2019
Hellenthal et al 2015
Souilmi et al 2020


Why does Stereology use Systematic Random Sampling?

Systematic sampling refers to a method where all samples have an equal probability of being chosen but the spacing between samples is constant. That is, although each individual section is equally likely to be chosen, the combination of samples is not. The Wikipedia article on systematic sampling provides a good overview.

Stereology refers to the analysis of a three-dimensional structure using two-dimensional slices. Such an approach is common with histological techniques. A block of tissue is sliced into thin sections that allow for examination of the tissue with light microscopy, usually with the aid of stains.

If you sampled purely randomly, by chance, you are likely to obtain "gaps" in your analysis by random chance. For example, imagine you section a 3mm block into 40um sections. This process gives you 75 sections. It is too time-consuming to analyze all 75 sections, so you want to choose just 15 of them.

Let's try generating 15 random numbers from 1 to 75 and look at the maximum gap. I do this by taking the first 15 numbers of a random permutation of 1 to 75. In MATLAB, one can do: x=randperm(75,15), max(diff(x));

Here are some results:

23    26    33    34    35    37    44    54    55    58    60    69    72    73    74

Max diff: 10

12    14    15    16    17    20    22    27    28    34    44    47    58    59    73

Max diff: 14

 8    14    15    18    19    20    29    32    40    41    47    67    70    71    72

Max diff: 20

 3     7    16    19    30    32    33    34    38    39    50    57    61    65    75

Max diff: 11

 3     7    17    18    21    26    29    37    42    46    49    52    60    61    69

Max diff: 10

If we were to instead use systematic sampling, the difference between sampled sections would be fixed at 5: you skip 4 sections to get 15 evenly spaced sections out of 75 total. But with purely random sampling, the largest gaps are bigger, sometimes much bigger! 20 skipped sections means there is a 800um gap with no data! Even worse, I noticed later that in the first draw, the lowest number was 23! So the first 22 sections are completely omitted from analysis! There can be major morphological changes and entire brain nuclei missed within a gap that size, whereas 100um gaps are no problem.

I didn't print out the minimum gaps, but you can look at my examples to see the other side of this problem: in the first set, numbers 33, 34, 35 and 72, 73, 74 are right in sequence! There is likely little or no morphological difference on those short intervals and yet with random sampling one can waste time analyzing those adjacent slices. Because these draws are completely random, you can notice similar adjacent stretches in all of these random draws, even though I made no effort to select particular examples: these are just the first 5 results I got from MATLAB.

References

Gundersen, H. J. G., & Jensen, E. B. (1987). The efficiency of systematic sampling in stereology and its prediction. Journal of microscopy, 147(3), 229-263.

Gundersen, H. J. G., Jensen, E. B. V., Kieu, K., & Nielsen, J. (1999). The efficiency of systematic sampling in stereology—reconsidered. Journal of microscopy, 193(3), 199-211.


It's a striped hyena, it is relatively rare/endangered these days. Hyenas are closer to cats/felines than to dogs. They are in the suborder Feliformia.
https://en.wikipedia.org/wiki/Striped_hyena
some images here


When does the brain stem appear in humans?

To correct the article you referenced the neural tube closure normally occurs by the fourth week of pregnancy (28th day after conception). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279093/

The Brainstem is comprised of three parts:

Medulla (Melincephalon)
The Pons (Metincephalon)
The Midbrain (Mesencephalon)

  During fetal development
  the brainstem is formed by:

  the myelencephalon (fifth vesicle) which will develop into the medulla (Melincephalon)
  the metencephalon (fourth vesicle) which will differentiate into the pons and cerebellum
  and the mesencephalon (midbrain)(third vesicle)

  An outline of the development of the brain stem is depicted in the image below:

  Pansky, B. 146. Introduction to Brainstem Development. Retrieved from https://discovery.lifemapsc.com/library/review-of-medical-embryology/chapter-146-introduction-to-brainstem-development

    By the end of the sixth week the rudimentary development of the five brain vesicles is complete. The cerebral hemispheres have grown and now cover the diencephalon, the mesencephalon and the cerebellum, which has only just begun development.

    Montfort, G. J., & Boon, R. Stages of Brain Development. Retrieved from https://www.bondingandbirth.org/uploads/5/4/1/5/5415260/06_stages_of_brain_development.pdf


The top is some kind of seal (the flippers give it away) and the bottom is some kind of lemur (the long thin limbs and tail with the narrow skull) but that is the best I can do from just those photos. It might be a flying lemur but again from just the one photo without scale is difficult to say for certain.


During human ageing, which immune cell sub-types are most affected?

From my Immunology notes:

*Decrease in hematopoietic stem cells resulting in a reduction of Affector cells. Erythroid and myeloid progeny cells don't seem to be affected.

*Fewer pro-B cells, resulting in fewer affector B-cells.

*Lymphoid progenitors in the bone marrow and thymus mature.

*Lymphocytes in secondary lymphoid organs.

For the Innate system:

*Neutrophils have a reduced capacity for Oxidative bursts, Batericidal activity, and Chemotaxis.

*Macrophages have a reduced capacity for phagocytic activity, oxidative bursts, and MHC II expression (which impairs their ability to present antigen and initiate CD4 Helper T-Cell responses).

*NK Cells have a reduced capacity for Cytotoxicity, proinflammatory cytokines and chemokines,and proliferation in response to IL-2. However, the total number of NK cells increases.

The sources: Both clinical (it was at a teaching hospital) and Aging and Immune System, Chapter 33 of the class text: Cellular and Molecular Immunology


Is there a difference between an organizer and inducer substance?

According to Merriam-Webster they are synonyms:

  [An organizer is]  a region of a developing embryo or a substance produced by such a region that is capable of inducing a specific type of development in undifferentiated tissue —called also inductor

Lifemap and Biology Today support the terms being synonymous as well.

However, I think the most commonly used terminology here is that the organizer [used as a noun] induces [used as a verb] the differentiation of embryonic tissue. For example, consider the following quote (Arizona State University):

  The Spemann-Mangold organizer, also known as the Spemann organizer, is
  a cluster of cells in the developing embryo of an amphibian that
  induces development of the central nervous system


Help identifying a bug which looks like a housefly and mosquito hybrid

This is a long-legged fly (Condylostylus spp).  Unfortunately your image is not sharp enough to give a specific species.  See this post of another Indian fly that is virtually identical to yours:
https://www.jungledragon.com/image/13762/long-legged_fly_-_condylostylus_spp.html


How might IV-saline cause kidney damage that seems to be less likely with "balanced fluids" IVs instead?

Short answer
There is not likely to be a single mechanism involved, but the study authors suggest that high chloride is the main issue; they refer to previous work showing a whole variety of issues that can be caused by higher-than-normal chloride levels.
Although saline contains roughly the same sodium content as blood plasma, it contains a lot more chloride than usual, because blood plasma contains several other anions such as bicarbonate.
However, please see the rest of my answer: this study shows a fairly modest effect and is certainly worth some more investigation but might not be as definitive as the news makes it seem.
The study in question
I assume the news article you reference refers to this recent paper:

Semler, M. W., Self, W. H., Wanderer, J. P., Ehrenfeld, J. M., Wang, L., Byrne, D. W., ... & Guillamondegui, O. D. (2018). Balanced crystalloids versus saline in critically ill adults. New England Journal of Medicine, 378(9), 829-839.

I am constantly befuddled by why journalism considers it appropriate to refer to a study with no citation at all of the original article, only barely noting one of the original authors and only after mentioning an interview with someone completely different. Even their link to "New England Journal of Medicine" is not a link to the journal but to other articles written by that news organization that also refer to NEJM.
Careful interpretation of the study results
First, note that this study is talking about a fairly small difference. It isn't like saline is causing people to just drop dead, and you recognize this in your question, writing:

Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt

Rather, the study showed that 1139/7924 (14.3%) with "balanced fluids" had an adverse kidney event versus 1211/7860 (15.4%) with saline.
They also reference two previous papers, one from the same authors:

Young P, Bailey M, Beasley R, et al. Effect of a buffered crystalloid solution vs saline on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA 2015;314:1701-1710.
Semler MW, Wanderer JP, Ehrenfeld JM, et al. Balanced crystalloids versus saline in the intensive care unit: the SALT randomized trial. Am J Respir Crit Care Med 2017;195:1362-1372.

each of which showed no difference between "balanced fluids" and saline.
Therefore, I think concluding

"...that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer."

is not necessarily true. In Young, et al., 102/1067 (9.6%) versus 94/1025 (9.2%) of patients showed signs of acute kidney injury for the "balanced" versus saline groups - a difference that was not significant (i.e., there are not enough subjects in the study to know that an effect this size is unlikely due to chance), but numerically the "balanced" group was worse. In Semler, et a. 2017, major adverse kidney events were 128/520 (24.6%) "balanced" versus 112/454 (24.7%) saline - literally as close to "no difference" as possible with this number of subjects (i.e., 111/454=24.4%).
Therefore, although this latest work shows a significant result with a larger population size, if you consider the previous work in this area the results are definitely mixed. The more recent Semler et al. 2018 paper's result is based on a p-value of 0.04, which is just below a commonly used threshold of 0.05 for deciding whether a result is significant. That doesn't mean the result is wrong, but it means that it should be considered in the context of other work being done in the area.
This study is also focused specifically on kidney issues, and although they have some other general secondary measures like deaths, the study is not designed or able to tell whether certain patients may actually be harmed by use of 'balanced' IV rather than saline IV.
To your actual question,
How might IV-saline cause kidney damage that seems to be less likely with “balanced fluids” IVs instead?:
The authors refer to other work showing that high chloride levels lead to a variety of issues; saline has a higher chloride level than normal blood plasma levels, so they suggest that if there is an issue with saline, the chloride levels are a likely cause, but this study has no ability to test those mechanisms.
Relevant quotes from the article, with emphasis mine:

In preclinical models, the high chloride content of saline has been reported to cause hyperchloremia, acidosis, inflammation, renal vasoconstriction, acute kidney injury, hypotension, and death. Studies involving healthy volunteers suggest saline may decrease renal perfusion through chloride-mediated renal vasoconstriction.


Cell type that expresses 90% of the genome

Well, I found this paper:
Danan-Gotthold M, Guyon C, Giraud M, Levanin EY, Abramson J. 2016. Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells. Genome Biol 17:219.

Medullary thymic epithelial cells [mTECs] express ~85 % of the entire coding genome
...to better determine the fraction of genes expressed in mTECs and other mouse tissues, we took advantage of RNA-seq technology... The analysis... revealed that most of the tissues [see below for those tested] express 12,000–14,000 genes (i.e. 60–65 % of the coding genome). The lung and two immunologically privileged sites, brain and testis, were the only tissues that expressed a larger fraction of the genome, in the range of 70–75 %... In line with other recently published studies, the mTEChi population expressed nearly 18,000 genes, which represents ~85 % of the coding genome, while Aire-deficient mTECs (AireKO) expressed approximately 15,000 genes, suggesting that Aire is responsible for the induction of ~3000 genes in mTECs. Interestingly, even in the absence of Aire, the mTECs expressed a relatively large fraction of the genome (~75 %), considerably exceeding the overall genome expression in other peripheral tissues. Interestingly, neither [cortical thymic epithelial cells] nor [skin epithelial cells] demonstrated higher overall genome expression than other tissues, suggesting that promiscuous gene expression is indeed unique to the mTECs population.

These cells express such a wide complement of proteins because they are involved in T-cell maturation, specifically negative selection.

List of tissues tested in the study:

brain, testes, liver, kidney, lung, colon, skeletal muscle, spleen, cortical thymic epithelial cells, skin epithelial cells


Determining whether X chromosome from sperm or egg

yes it is possible... in placenta (trophectoderm) the paternal X is epigenetically silenced [ref].

That is if you do the test in the pre/neo-natal stage. Otherwise, at later stages, you have to check by DNA fingerprinting + karyotyping/FISH as Chris suggested.


You trespass upon a question as old as antiquity: what properties constitute consciousness? The best means to respond to the question concerns a metaphysical answer and an answer in modern biology

We can perhaps divide consciousness into two categories: contiguous thought from past experience and identity and secondly, self-awareness.

The reputed example of the Sorites problem of Theseus' Ship describes how the physical entity of Theseus' ship, during his various battles and broils, loses certain components of his ship: his braces or mast, in example. They are replaced with exact replicates until the time that every component of the ship has been supplanted by a replaced component. Is it the same ship? It is dependent on your definition of identity.

Leibniz's Law of Identity whether in humans, ships or spaghetti monsters, states that objects x and y hold the same identity if and only if they share all the same predicates - qualities or attributes. If this be of functionality, the ship completes the same function and comprises the same components, albeit of different origin - thus, the ship has the same identity. This is important regarding your question whether your 'old [you] dies'. Over time, your cells undergo mitosis and eventually apoptosis. Hence, although your parts are in constant flux, the predicates between your old self and latter self are constant. Ideologically however, there is no set identity!

If you read David Hume's literature, you will observe the notion that one is only the composition of impressions (sensory reception) and thus there exists no identity.

Your question regarding clones is a challenge for biology. Behaviourism is an approach in biology concerning the interpretation of behaviour as a response to a stimulus. Furthermore, humans express complex instinctive behaviours in response to various stimuli. If there exists no 'mental substance' distinct from the body, then it seems plausible to consider human consciousness merely an extension of an advanced instinctive epiphenomenon: self-awareness is a by-product to these advanced behavioural patterns. To support this position, simply recall what factors allow one to discriminate individuals whom one meets, behavioural patterns and appearance.

Finally, one could attempt to assess consciousness in regard to self-awareness by conducting the mirror assessment. If one is capable of identifying himself/herself, then it is indicative of an ability to discern one's personal existence from general matter.

This is by no means a comprehensive answer to this question yet I bid you well in your continued explorations of human consciousness.


How well does it actually work to surgically reroute the optical nerve?

At least two follow-up studies have investigated the behavioral consequences of the re-routing of the optic nerve to the auditory cortex. In these animals the visual cortices were ablated, and the optic nerve re-routed by combined lesions of the superior colliculus and ascending auditory pathways to the thalamus. These lesions induce retinal axons to form permanent ectopic (i.e., re-routed) projections to the auditory thalamus and cortex. These ectopic visual projections result in the formation of retinotopic maps in the auditory cortex and in visually responsive neurons with receptive field properties reminiscent of cells in the visual cortex.

These re-wired ferrets and hamsters were shown to have functional vision, as shown by their ability to tell light from dark and to recognize simple visual patterns. Visual pattern recognition was absent in control animals that were blinded, but not re-wired. Visual function, as measured by grating visual acuity in re-wired hamsters and rats, was however not as good as in control animals with normal vision (Frost et al., 2000; Melchner et al., 2000).

References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Melchner et al., Nature (2000); 404: 971-6


Shannon diversity index: Pi relates to all found species, or number of species by site?

I am trying to dig into Shannon's species diversity index to compare the species diversity between different sites

Shannon's diversity index is a measure of alpha diversity, or diversity within a community. If you are considering each site a different community (which is sounds like you are), then you would calculate Shannon diversity for each site separately, without consideration of the other sites.

What I do not understand is if this relative abundance relates to all species in a sample, or all found species?

Relative abundance is not a function of the number of species found, but the total number of observations collected (similar to sampling effort) at a given site. So, if you made 100 total observations at a site and 10 of those belonged to Species X, the relative (proportional) abundance of Species X is (10 / 100) or 0.1, regardless of the total number of different species present, and regardless of any observations from other sites.
I can't comment on your code, because I don't do tidy-verse. I guess I'm (apparently) old school and still use Vegan and LabDSV for community analysis (I may be biased since I learned community ecology from the author of the LabDSV package). But in general, for any measure of alpha-diversity, each community gets it's own value, and you would not consider any observations from other sites in that calculation, regardless of whether there is species overlap between communities.
For a more direct comparison of diversity between sites, you would use a beta-diversity index like Bray-Curtis dissimilarity, which compares each community to every other community in your analysis.


Involuntary twitches and apnoea during early phases of sleep

Jerk-like muscle contractions occurring while drifting off to sleep are normal and are referred to as "sleep starts" or sleep myoclonus (National Institute of Health - NINDS).

Sleep Education explains the symptoms:

  Sleep starts usually consist of one strong jerk that affects much of the body. The arms and legs are most likely to be affected.

So sleep starts may be quite vigorous, but may consist just of small lip movements too.

The American Sleep Association mentions that:

  Sleep myoclonus will rarely disturb the subject or any bed partner to the point of waking and disrupting sleep [...].

In fact, sleep starts are associated with tachypnea, i.e., an increased in breath rate (Vetrugno & Montagna, 2011)

Hence, your hypothesis that a myoclonus is a mechanism to wake a person up (for whatever reason) seems unsupported.

Reference
- Vetrugno & Montagna, Sleep Medicine 2011; 12: S11–S16


So I think this is a more conversational kind of question. I will address some misconceptions you have, and I will try to keep it brief, considering the nature and depth of your question. One could comment on the question very deeply, so I'll stick to addressing some misconceptions.

  Can I tell whether my sandwich is contaminated for example?

Usually you can taste contamination because of the (action of) metabolic products of microorganisms. You do not taste nor smell the microorganism directly; you taste their metabolites or the effect of their presence, such as products of fermentation, or oxidized molecules which are normally not present because air does not penetrate through e.g. apple skins. Take filamentous fungi, for instance; they release enzymes that act on complex carbohydrates to break them down. You cannot taste the cellulose which makes up the majority of a stalk of celery, but you may be able to taste its broken down products once a fungus has begun to digest it prior to absorbing its nutrients: sweet glucose, sucrose, trioses, some acids. It depends on the food and the extent and kind of contamination.

  they are too small to have any taste and, even if you manage to eat a whole lot of viruses it would taste like water.

You can taste molecules which are far smaller than a virus. Indeed, pheromones and volatile or sticky chemicals and all that jazz are definitely much smaller than viruses. Viral particles themselves may actually be too big to taste, because your sense of gustation and olfaction depends on the interaction between tastant or odorant molecules and corresponding receptors, which are situated on the membrane of sensory neurons (nerve cells which are responsible for detecting and relaying information to the brain about the outside world). These receptors harbor ligand-binding pockets that are too small to capture entire viruses. This does not rule out the ability for you to taste broken bits of viruses, but I think this is unlikely or coincidental (i.e. the particle may bind to receptors weakly and not very well).

  it would taste like water

Water is a requisite for taste and smell, things have to be dissolved in water for you to be able to detect them. Water by itself has no taste! Only impurities, oxygenation and carbonation and mineral content give water flavor. I understand that you factor in temperature and texture into the 'perception of water', but these are not gustatory phenomena and use different mechanisms of detection.


Bistability referrers to two coexisting stable conditions (if you disrupt they will tend to restore to one of those two areas) and has a slightly broader application it can also involve chemical stability for instance. Bistability includes the element of stability (obvious in the name) if disrupted bistable condition tend to return to one of two stable configurations. Enzyme stable configurations could be another. Galapagos finch beak shape during wet years is the one I think of but that could also be argued as tri-stable. to go really simple you can even think of a clicky pen, fully clicked is stable and unclicked is stable but anything else immediately moves to one of the other states.

Bimodal just means the distribution has two peaks, they may or may not be stable, many are only temporary. It is a much simpler concept.

Another way to consider it is bimodal is purely descriptive while bistability has a predictive quality.


Apparently not, leakiness can be controlled by tightly regulating the T7 polymerase with a tight promoter (in this case lacUV5).


Large black caterpillar, cocoon, moth - Los Angeles

Based on the image of the moth, I think this is a Painted Tiger Moth (Arachnis picta). See the image of the moth from the Wikipedia (you can even see the yellow color at the head region):

An image of the caterpillar can be found here, but this is less decisive.
It also fits with the geographic location where you found the moth, see here.


Why does the seed of the coconut tree have a liquid in it?

It is a transitory state.

During coconut development the "milk" actually starts as a spongy solid a multinucleate endosperm. As the coconut develops it absorbs this tissue. Because of a coconuts hard structure this leaves a cavity since the coconut cannot change shape as the tissue density changes, some fluids including oils are left behind as hte tissue is broken down and reabsorbed. But this fluid will be reabsorbed as the the developing cotyledon fills in the cavity. The fluid is a by product of the cavity but the the cavity is needed due to the unusual development of the coconut.

As a side note most comercial coconut milk is actually squeezed out of the solid endosperm.


Why does opening of the Ca-channels trigger the release of neurotransmitters?

Synaptotagmin is a protein that is part of the synaptic release machinery. It binds calcium specifically, which leads to a conformational change that encourages vesicle fusion with the membrane, therefore the ultimate release mechanism is not via voltage or charge but by calcium itself.


What kind of spider is this? I have never seen one like this before

On iNaturalist I found a very similar picture, of a White-Banded Crab Spider.  It is found in your area.  It's a possibility.


How could 45 milligrams of a substance equal 4,500 micrograms?

This is a typo.  In the text he states:

  ... only 0.120 milligrams (120 micrograms) of MK-4 ...

So, he knows the correct conversion.

Then:

  ... the "same" product is almost 40 times more potent in one country
  ...

40 times 120 micrograms is 4800 micrograms -- which is close to 4500.

So, that suggests that the (4,500 micrograms) in the table is correct and that the 45 milligrams is a typo.

It should read 4.5 milligrams.


How do I score differential activity of cellular pathways in microarray data (not enrichment)?

You would look at downstream genes, which are selective for individual pathways - or genes which have binding sites for transcription factors that sit at the end of your pathway. Depending on the existing literature, and your experiment, and the specific pathway, this can include genes, which are themselves part of the pathway (if feedback). For interpretability you would prefer genes, which have previously been established as makers of a pathway in preceding literature.

  I would like to identify cellular pathways (KEGG) with discriminative changes in the average activity (expression levels) of their gene members in a two-condition microarray dataset.

This might be tricky, since the taking the average introduces several assumptions such as: little impact of technical background (expression of most genes of pathway above background), average being representative of the KEGG pathway of interest (and not only of the most abundant pathway members), and enforcing a somewhat arbitrary decision of whether to average log-transformed data (which is justified for many genes, but not genes that don't scale multiplicatively, such as many stress genes), or not log-transforming.

  The goal is to use the average pathway activity for machine learning (sample classification),

You can use this to your advantage, and create multiple features per pathway (e.g.: median, mean, variance, non/log-transformed etc..., manually -curated signature genes of pathways), and then having machine learning choose the best features for your classification (e.g.: as would happen if using Random Forest Classifiers)


Text Book Recommendation: Organic Evolution

Organic Evolution - Definition

'Organic evolution' was a common term. It is just rarely used today. Today, we just say 'evolution' or 'evolutionary biology' when referring to the field of study of 'evolution' (or of study of 'evolutionary processes').

Book recommendation

Math oriented

As you are used to work in applied mathematics, you'll definitely be interested in an intro book to population / evolutionary genetics. Population genetics is the mathematical basis of evolutionary theory. You will find recommendations at the post Books on population or evolutionary genetics?.

For you, I'd recommend Population Genetics: A Concise Guide as a start (or another one presented in the first section of the top answer to the post I referred to above). If then, you like coalescent theory (branching process), you might want to look at Coalescent Theory: an Introduction or some other more specialized books.

Not Math Oriented

Maybe you'll want something more introductory with much less math such as the Evolution: Making sense of life by Zimmer and Emlen or Evolution by Futuyma. These books are classic textbooks for intro class to evolutionary biology in Bachelor. These books will have the advantage to present you some other subfields of evolutionary biology such as the diversity of life, reading phylogenetic trees, ecological relationships and many other things that the books of population genetics don't go over.

Most common fields of math used in evolutionary biology

The most common fields of mathematics used in evolutionary biology are system dynamics, game theory, approximation theory, probability theory, branching processes and diffusion equations.


Why can't a human regenerate limbs like some other species?

After salamanders (or certain other amphibians) lose a limb, the epidermis migrates to cover the wound, forming a structure known as the apical epidermal cap. The underlying "stump" then generates a de-differentiated mass of cells from normal tissue. In most cases, these cells will express genes that are vital to the proper formation of limbs, such as HOX genes. This "lump" of cells at the stump of the wound are typically referred to as a blastema. Basically, the blastema continues to grow and regenerate the limb in a way similar to fetal growth. Though mammals (including humans) also have some regenerative capabilities, they are much more limited. In addition, many regenerated limbs will also be mildly deformed (square fingernails). In axolotl salamanders, it was found that certain retrotransposons, such as the LINE-1 element, were prevented from "jumping" around in the developing blastema during limb regeneration. The two active proteins PL1 and PL2 were responsible for inhibiting the activity of LINE-1 and other such retrotransposons. Active retrotransposons can potentially rearrange the genes in germ cells can be detrimental to the mechanisms that allow the blastema to replicate and differentiate, so the PL2 and PL1 proteins play a vital role in their regenerative capabilities. When the PL2 and PL1 proteins were "switched off" in certain axolotl salamanders, their regeneration was much less efficient. Since mammals lack the PL1 and PL2 proteins and have a different LINE-1 retrotransposon, they have reduced regenerative capabilities.

Sources:

Wei Zhu, Dwight Kuo, Jason Nathanson, Akira Satoh, Gerald M. Pao, Gene W. Yeo, Susan V. Bryant, S. Randal Voss, David M. Gardiner, Tony Hunter. Retrotransposon long interspersed nucleotide element-1 (LINE-1) is activated during salamander limb regeneration. Development, Growth & Differentiation, 2012; 54 (7)

Wei Zhu, Gerald M. Pao, Akira Satoh, Gillian Cummings, James R. Monaghan, Timothy T. Harkins, Susan V. Bryant, S. Randal Voss, David M. Gardiner, Tony Hunter. Activation of germline-specific genes is required for limb regeneration in the Mexican axolotl. Developmental Biology, 2012; 370 (1)

Odelberg SJ (August 2004). "Unraveling the Molecular Basis for Regenerative Cellular Plasticity". PLoS Biology 2 (8)


Methylation is increasingly seen as a consequence of gene activity rather than a regulatory mechanism. There are cases where methylation is controlled because of gene regulatory control, especially at the famous H19/Igf2 locus[1]. Here is a generally good recent review[2], note they mention that DNA methylation does not cause transcriptional silencing, and likely methylated promoters are probably more active than unmethylated, they just create silencing RNAs when methylated (resulting in an apparent silencing).  This may help explain some of the story[3], but note how old that paper is, yet generally I'd say few people know of its existance.

The exception seems to be transposable elements[4], but their control is probably also controlled by silencing RNAs.

References:

 Zampieri M, Guastafierro T, Calabrese R, Ciccarone F, Bacalini MG, Reale A, Perilli M, Passananti C, Caiafa P. 2012. ADP-ribose polymers localized on Ctcf-Parp1-Dnmt1 complex prevent methylation of Ctcf target sites. The Biochemical journal 441: 645–52.
 Deaton AM, Bird A. 2011. CpG islands and the regulation of transcription. Genes & development 25: 1010–22.
 Rountree MR, Selker EU. 1997. DNA methylation inhibits elongation but not initiation of transcription in Neurospora crassa. Genes & Development 11: 2383–2395.
 Bourc’his D, Bestor TH. 2004. Meiotic catastrophe and retrotransposon reactivation in male germ cells lacking Dnmt3L. Nature 431: 96–9.


Using anatomical terms for human organs and parts of plants

First, for reference, see here for a discussion about the difference in directional terms between bipeds and quadrupeds as well as a fairly complete explanation of word meanings/etymology.

The etymological meanings of the various anatomical directional terms should help explain their usage in body organs. For example:

Ventral -> "belly" side
Dorsal -> "back" side
Anterior -> "before" or "toward the front"
Posterior -> "after" or coming after (opposite to) the anterior

For body organs (or other body parts):

This SE question addresses hands and feet, while this page from Bryn Mawr College directly demonstrates the usage of anatomical positional terms of the brain:

Rostral/ Anterior --->   Head or front end
Caudal/ Posterior --->  Tail or hind end
Dorsal  --->    Back or top side
Ventral --->    Belly or bottom side

Anatomical positional terminology for brains is consistent across organisms. Here is another picture demonstrating anatomical positional terminology of this organ from Santa Monica college:

For plants, see "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

  Dorsal. Pertaining to the back or outward surface of an organ in relation to the axis, as in the lower surface of a leaf; abaxial. Figure 407.

  Ventral. Pertaining to the front or inward surface of an organ in relation to the axis, as in the upper surface of a leaf; adaxial. Figure 1428.

Therefore, dorsal/ventral are determined relative to the axis of where the leaf connects to the stem (ie., the axil). Because of this, in my experience terms such as abaxial and adaxial would be preferred when referring to plants.


How does the cornea breathe during sleep?

As you noted, the cornea needs oxygen, yet it's not vascular. It needs to get it's oxygen supply from diffusion. In the daytime, diffusion occurs from air through the tear film covering the cornea.

The cornea spends about a third of it's lifetime under closed lids. At night, the tear film remains intact and is continuously replenished. The inner aspect of your eyelids, called the palpebral conjunctiva, are highly vascularized, with capillaries just below the surface (and accessory tear ducts and tiny mucosal glands to keep it moist).

When you sleep, oxygen (and nutrients) diffuses from the palpebral conjunctival capillaries through the tear film to your cornea.

The blood vessels in the palpebral conjunctiva are more permeable than most other capillaries and contribute fluid and nutrients to tears by leaking plasma. The surface epithelial cells are also a source of tear fluid because of a special arrangement of the cells such that there is more intercellular space allowing fluid, antibodies, and other plasma constituents to the surface of the conjunctiva.

This very issue was of great concern to ophthalmologists when people started wearing extended-wear contact lenses.

The Conjunctiva and Lacrimal System (www.eyecalcs.com/DWAN/pages)
Organization of Capillaries in the Primate Conjunctiva
The Conjunctiva—Structure and Function (oftalmologia/enciclopedias)
The oxygen tension and temperature of the superior palpebral conjunctiva
Facts About the Cornea and Corneal Disease (cool article)


What is the correct medical procedure(s) for taking a resting heart rate?

1) According to this article you should be taking it in the most preferred position you want. It would change according to the position you are in so make yourself comfortable sitting or lying down (reference).

2) You take the number of beats of your heart in a minute. If you take the number of beats for 2 minutes, then average your count by 2.

3) One minute (reference).

4) Completely relaxed, most articles recommend taking it in the morning while waking up so you are doing the right thing (reference).

I don't understand what you mean by an academic situation so I could try and answer it if you clarified it.


In the big cities of North America (e.g N.Y), the big piles of dirt and moisture attract many hostile animals such as the ones you mentioned: the cockroaches. You should also consider that in the north there is a very common factor that attracts collonies of cockroaches: the low to mediocre temperatures. Moreover, you should reconsider the cleanliness of the sewers. The sewer and the leftovers that exist there are highly nutritional for the cockroaches. That's why you don't see many dead ones on the streets. And where is the start of the sewers? The sewers start from every house. That's why you notice more roaches in the houses than outdoors. They need a place that might provide them the sewer's environment such as the bathrooms, or an other place in the house that has moisture and is mostly dark. Cockroaches live and die to the same place and don't go somewhere else to die. The decay rate outdoors is higher of course, than indoors because every house is cleaner than the roads. With the process of cleaning many factors, such as mites are swept away to the environment.

For the second part of your question:

Outdoors there are many  scavengers and natural predators for the cockroaches. Some of them are: toads, frogs, beetles, geckos, iguanas and birds.  Entomopathogenic fungi have also been identified as lethal to roaches, as their spores attach to insects and kill them within weeks. Cockroaches affected by fungi then pass the parasite on to other cockroaches, and the cycle continues.

Ants prey on some cockroach species, but other roachess actually live with ants in their colonies. These are called myrmecophiles, meaning lovers of ants. They don't seem to offer their hosts anything in return for living with them, and are usually tiny and unobtrusive. Other species - termitophiles - live in similar fashion with termites.

And yes ants are the major factor of dicomposion in nature, because they devour almost anything.

I hope this answered your question, becaused I used very extended research :)


What is the reason behind choosing the reporter gene when experimenting on your gene of interest?

Different genes will serve different purposes. For example, if you want to perform colocalization studies, then fluorescent genes like eGFP and DS-Red (or any variation of those, namely Emerald, mCherry, etc) will be quite useful, since you can use different filters on your microscope for the various fluorophores. For morphological assessments, perhaps a LacZ gene or alkaline phosphatase may be better suited, since the detection of these enzymes is compatible with standard histological techniques and you get usually much better contrast than with fluorescence. For quantification purposes, you would use probably firefly luciferase or CAT, since there are very good quantitative assays for these enzymes.

The decision will also depend on the degree of experience of the lab with each detection technique and even in the availability of the constructs. If a reporter is already made by the lab next door and if it fits your needs, you'll just use it, instead of creating your own, even if the reporter gene would not have been your first choice.


What is this creepy little thing that I found sticking on my bathroom wall?

This is the pupal stage of a lepidopteran (i.e. a butterfly/moth). The pupa is encased in the brown silken cocoon in the centre of the 'net'. The 'net' itself is built from the setae (hairs) of the caterpillar, which it sheds prior to cocoon formation.
Here's some photos of similar formations:

http://www.richard-seaman.com/Insects/Vietnam/Highlights/index.html#Chrysalis
https://www.nhm.ac.uk/wpy/gallery/2019-the-hairnet-cocoon?tags=ed.current
https://besgroup.org/2015/11/05/a-parasitic-fly-emerged-from-the-cocoon-of-a-footman-moth/


It would help if you could delimit in which cellular of molecular context you would like to understand packing defect, for exemple during vesicular budding or lipid droplet biogenesis.

In the larger context of cellular membranes lipid packing defect occurs when there are transient "holes" made in the phophosolipid bilayer.

These packing defects can be caused by the chemical nature of the phospholipids present in the membrane. A phospholipid is chemically defined as an amphiphilic molecule: it contains a hydrophilic head and an hydrophobic tail.
The head size can vary a lot between the different possibles groups (serine, choline, ethanolamine, etc).
The size of the hydrophobic tail which is composed of long carbon chains can vary in length (typically 16-18 carbon atoms) and saturation. The saturation is very important because insaturated lipids (16:1, 18:1) tends to have to be kinked where the insaturation is.

Thus depending on the lipid composition of the membrane, it is possible to have micro domains (previously named lipid rafts) composed of only a specific lipid or group of lipid with a defined molecular composition. Packaging defects which called be name "holes" or imperfections in the membrane might occur at the boundaries of these microdomains because of the difference of the head size, length of the fatty acid chain, and saturation.

Many people also think that proteins can be responsible for the segregation of chemically defined lipids in the membrane and cause packaging defects for exemple proteins with an hairpin structure instead of a transmembrane domain, or proteins which interact with membranes with an amphipathic helix.

I hope this helps!


These new GO terms seem to be the parents of the already GO terms present in my original dataset.


that's the stated purpose of the thousand genomes project.

the thousand genomes project has.. 1000 genomes.

its all downloadable.

http://www.1000genomes.org/


Is pulse rate measurable in the capillary bed and venous vasculature?

In the capillary bed? Absolutely! In the venous return? Depends!

I had to build one of these for class. In short: you can tell how oxygenated the blood is by its color, but you have to correct for how much blood there is: The dilation of the arterioles and capillaries with the heartbeat increases the size of the area being measured, and changes all sorts of properties including conductance. There's a neat heartbeat monitoring method method that involves putting two electrodes on your arm, one at the wrist and one at the elbow, and measuring the increase in conductivity every time your heart beats and your arm swells.

Depending on heart rate and all sorts of other things, there's not usually a detectable heartbeat in the veins right outside the heart (see the CVP, which is pretty much flat). However, the jugular venous pressure is the pressure of the internal jugular vein that drains the head, and that has heartbeat oscillations (not one-to-one, there are "echoes" and other weirdnesses because it's almost connected to the heart. See here for more).

In sum: The capillary bed absolutely swells and contracts with each heartbeat, but in the veins blood usually just oozes along. There are a couple exceptions but mostly they're silent.

(The Korotkoff sounds you're talking about are a fluid dynamics thing. When the veins are regular-sized they're wide enough to permit laminar flow(where all the blood moves in a straight line), which is smooth but still pulsatile. Like these guys the blood flow starts and stops but is in sync with itself. When you compress them you increase the Reynolds number and you get turbulent flow, which you can hear because it's making noise.)


Is there any way a human could whistle and be unable to speak?

Short answer(s)
Someone with a damaged larynx may still speak with the use of a speech aid (electronic larynx).

The ability to understand speech does not necessarily mean one can speak normally. There are neurological disorders where folks can understand speech, but have difficulty producing it.

Background
A full removal of the larynx (laryngectomy) prevents the patient to produce speech because the vocal chords are removed. However, with the use of a voice prosthesis this can be solved (Cancer Research UK).

There are neurological disorders where one can still understand speech, but has impaired ability to generate it, called apraxia. Apraxia can be acquired or congenital (developmental) (NIH). The developmental type is not well understood a the neural level (Dyspraxia Foundation UK). The acquired type is known to occur through damage to specific brain areas, for example due to trauma or stroke. One of these areas associated with acquired apraxia is Broca's area (Graff-Radford et al., 2014), which is a brain area intimately associated with the production of speech .

Broca's area. Source: UC Irvine

However, although damage to this area can result in pure apraxia (i.e., impaired speech but normal speech understanding), it can also result in Broca's aphasia, which means that language understanding is also impaired (American Heart Association). Moreover, regarding your specific question, apraxia is characterized by impaired speech, but not a total lack of speech production.

Reference
Graff-Radford et al. Brain & Language 2014;129:43–6


Why are canines not nauseated by similar foodstuffs/state of decay as human beings?

Your dog finds these things palatable, I assure you, and no gag-reflex suppression is needed.

I had a dog that would steal duck eggs from my flock, bury them all over the place, and dig them up when properly rotted to enjoy as a treat, and no, I'm not making this up. I saw her do it, ran across many buried duck eggs while gardening, and could immediately smell when she was enjoying one.

All that to say what smells good to a dog has nothing to do with what is acceptable to you. Many of your "dislikes" are conditioned: living in a society where cleanliness is valued and clean water is available, humans in such societies can afford to snub their noses at less sanitized things.

Manure may well elicit a completely different reaction to a farmer, who saves it carefully before spreading it on his fields to enrich the soil. To him, it might be the smell of a good crop next summer.

Many species exhibit corprophagia. It's not known why dogs (some, far from all) do this. Rabbits, for instance, eat their own feces after their first movement of the day. This is normal and nutritional for them.

Eating the feces of other species, particularly herbivores, is common among dogs and isn’t considered abnormal, just undesirable. My (same) dog followed my goats around like they were Pez dispensers. Since dogs can't digest cellulose, they get some of the advantage of eating plants this way.

Capybara, rabbits, hamsters and other related species do not have a complex ruminant digestive system. Instead they extract more nutrition from grass by giving their food a second pass through the gut. Soft fecal pellets of partially digested food are excreted and generally consumed immediately. Consuming these cecotropes is important for adequate nutritional intake of Vitamin B12. They also produce normal droppings, which are not eaten.

Young elephants, pandas, koalas, and hippos eat the feces of their mother to obtain the bacteria required to properly digest vegetation found on the savanna and in the jungle. When they are born, their intestines do not contain these bacteria (they are completely sterile). Without them, they would be unable to obtain any nutritional value from plants.

Eating garbage and human feces is thought to be one function of dogs during their early domestication, some 12,000 to 15,000 years ago. They served as our first waste management workers, helping to keep the areas around human settlements clean. A study of village dogs in Zimbabwe revealed that feces made up about 25% of the dogs’ overall diet, with human feces making up a large part of that percentage.

Coprophagia
Daily rhythms of food intake and feces reingestion in the degu, an herbivorous Chilean rodent: optimizing digestion through coprophagy
Coprophagia as seen in Thoroughbred Foals


I would caution you against using phrases such as "completely cured" or even "cured". This goes beyond our technical ability to detect the presence of tumor cells within someone's body. All we can conclude is progression-free survival (i.e. living with cancer that does not get worse) or disease-free survival (i.e.  or no signs or symptoms of the tumor). Many of these data are included in cancer trials along with overall survival rates. Some general statistics for many groups of cancers can be found here: http://www.cancer.gov/statistics/find

And a glossary of terms used in reporting cancer statistics here: http://www.cancer.gov/statistics/glossary


How to annotate a .broadpeak file with 9 columns?

This is what the columns of broadPeak format mean (from UCSC):

  chrom - Name of the chromosome (or contig, scaffold, etc.).
  chromStart - The starting position of the feature in the chromosome    or scaffold. The first base in a chromosome is numbered 0.
  chromEnd - The ending position of the feature in the chromosome or   scaffold. The chromEnd base is not included in the display of the    feature. For example, the first 100 bases of a chromosome are defined
  as chromStart=0, chromEnd=100, and span the bases numbered 0-99. If
  all scores were '0' when the data were submitted to the DCC, the DCC
  assigned scores 1-1000 based on signal value. Ideally the average  signalValue per base spread is between 100-1000.
  name - Name given to a region (preferably unique). Use '.' if no name is assigned.
  score - Indicates how dark the peak will be displayed in the browser (0-1000).
  strand - +/- to denote strand or orientation (whenever applicable).    Use '.' if no orientation is assigned.
  signalValue - Measurement of overall (usually, average) enrichment for the region.
  pValue - Measurement of statistical significance (-log10). Use -1 if    no pValue is assigned.
  qValue - Measurement of statistical significance using false    discovery rate (-log10). Use -1 if no qValue is assigned.

And this is how the BED format looks like (from UCSC):

  chrom - The name of the chromosome (e.g. chr3, chrY, chr2_random) or    scaffold (e.g. scaffold10671)
  chromStart - The starting position of the feature in the chromosome    or scaffold. The first base in a chromosome is numbered 0.
  chromEnd - The ending position of the feature in the chromosome or    scaffold. The chromEnd base is not included in the display of the feature. For example, the first 100 bases of a chromosome are defined
  as chromStart=0, chromEnd=100, and span the bases numbered 0-99.
  name - Defines the name of the BED line. This label is displayed to    the left of the BED line in the Genome Browser window when the track is open to full display mode or directly to the left of the item in pack mode.
  score - A score between 0 and 1000. If the track line useScore attribute is set to 1 for this annotation data set, the score value will determine the level of gray in which this feature is displayed (higher numbers = darker gray).
  strand - Defines the strand - either '+' or '-'.
  thickStart - The starting position at which the feature is drawn    thickly (for example, the start codon in gene displays). When there is no thick part, thickStart and thickEnd are usually set to the chromStart position.
  thickEnd - The ending position at which the feature is drawn thickly    (for example, the stop codon in gene displays).
  itemRgb - An RGB value of the form R,G,B (e.g. 255,0,0). If the track    line itemRgb attribute is set to "On", this RBG value will
  determine    the display color of the data contained in this BED line.
  NOTE: It is    recommended that a simple color scheme (eight colors or
  less) be used    with this attribute to avoid overwhelming the color
  resources of the    Genome Browser and your Internet browser.
  blockCount - The number of blocks (exons) in the BED line.
  blockSizes - A comma-separated list of the block sizes. The number of items in this list should correspond to blockCount.
  blockStarts - A comma-separated list of block starts. All of the blockStart positions should be calculated relative to chromStart. The number of items in this list should correspond to blockCount.

So, first six columns are basically the same. The 7th and 8th column of your new BED file should be same as 3rd and 4th columns respectively. Since columns 4-12 are actually optional for a BED file you need not actually fill the rest of the columns. In any case blockCount would be zero for your case. RGB value is also not necessary. However, if whatever software you are using is asking for a 12 column file then set these:

itemRGB (column 9) = 0,0,0 (black)
blockCount (column 10) = 0

You can use whitespace in rest of the two columns.

You can easily use any scripting language to do this. I am not going to explain how to do that because that is off-topic here.

How to find nearest genes without using Peakanalyzer?

Download the GENCODE annotation GTF file and decompress it.
Read the broadPeak file and store the locations of the peaks.
Define what the minimum level of proximity is (for e.g. 2kbp up/downstream)
Parse only those lines of the GTF where the third column="gene"
Subtract the downstream window to start and add the upstream window to stop position of the gene. Columns 4 and 5 respectively.
Gene information is stored in 9th column.
If the stored peak position falls within the modified start/stop positions then print the 9th column.

Again, this is has to be done programmatically. It is not very difficult. To explain how to do that is off-topic in this forum. I explained the algorithm which you can implement in your favourite scripting language.


I will assume the hand washing you speak of involves soap.

The human skin (which also covers hands) is a complex organ with an underlying system of glands.

One of these is the exocrine sebaceous gland which is responsible for the production of a substance known as sebum. This substance is primarily composed of triglycerides, wax esters and other fatty acids. Sebum makes human skin waterproof as it's constituents are not water soluble (oily).

The action of soap on oily substances typically involves increasing their solubility in water so that they can be easily rinsed upon being dissolved. So when one washes their hands with soap they remove the oil layer secreted by the glands under their skin.

Removing the oil layer makes the skin susceptible to drying up as oil reduces the rate of evaporation of water on the skin to maintain a moisture balance. This is the reason why most brands of lotion have a moisturizing effect (or marketing statement).


How do you find pre-miRNAs from mature miRNA Blast output?

DISCLAIMER: I have never worked with miRNAs.

However, from what little I know, the mature miRNA is produced by modifying the pre-miRNA. This means that you should be able to infer the pre-miRNA by mapping your miRNA to the genome using a tool like BLAT. Since you already have an EST which represents a transcribed sequence, you can map your EST back to the genome. You can simplify this by using a tool like exonerate that also models splicing.


So in a pedigree, Standardized Human Pedigree Nomenclature: Update and Assessment of the Recommendations of the National Society of Genetic Counselors notes that these "nodes" in the pedigree are the "individual symbol" denoting individuals. Although, when you read it, you'd read "Male," "Female," "Gender Unspecified," etc. instead of individual symbol.


Do ant pheromones indicate the direction to go?

@shigeta is correct.  Trail disruption is actually a method of controlling ant populations.

For an example, see http://www.ncbi.nlm.nih.gov/pubmed/20077128


Problem on number of amino acids that an alien can use

I also got 624. Maybe the answer is incorrect.
My processing is:

Each codon has four bases, the species contain five unique nucleotides, so for the first position in the codon, there are 5 possible results, also, for the second position in the codon, there are 5 possible results, it is same in third and forth position,

so the result should be  5*5*5*5-1=624


Essentially, yes. These tests are usually based on enzymes that replicate DNA, and they have a certain (small) probability of getting a base wrong now and then. You can estimate the error frequency by doing many repetitions of sequencing of the same DNA sample and counting the number of discrepancies. Of course, this assumes that there are no systematic errors, only random variation, which may not be entirely true.

The Sanger sequencing technique is estimated to have error rates on the order of 0.001% (or, is 99.999% correct). I don't know exactly how these firms calculate their numbers, but I would guess it is similar.


How do our sensory organs work automatically without our conscious effort?

Because consciousness evolved much much later than sense organs, and consciously seeing does not make much sense evolutionarily speaking.
We can consciously direct some sense organs, like the eyes, but signals sent sense organs by their very nature have to activated by outside stimuli otherwise they don't work as sense organs. If I could command my taste buds to taste cheese pizza while eating hay or poison it kinda defeats the purpose of having taste buds in the first place.
You really don't tell most of your body to do anything it happens automatically, becasue there is no benefit to doing it consciously, humans have more ability for fine motor control of some muscles becasue they help with things like speech or tool making, but having to learn to consciously control pupil dilation would take much longer and likely result in quite a bit of damage to the eye.
Now our eyes do have to learn how to see (or at least how to focus) and our brain has to learn how to interpret the impulses from our sense organs, but this is not really conscious learning. there is a cool experiment you can to to reteach your brain wrong see the inverted vision experiment but all the learning is without you being aware of it.


What is known about the coding sequence of Factor H in the human genome?

As clearly stated in the WP article:

  The molecule is made up of 20 complement control protein (CCP) modules (also referred to as Short Consensus Repeats or sushi domains) connected to one another by short linkers (of between three and eight amino acid residues) and arranged in an extended head to tail fashion.

So in your terminology yes, it is a repeat cluster. Each of those 20 domains will be similar to the others, although not identical.


Do mammals develop tolerance to anticholinergics?

The tolerance to antihistamines is an ongoing debate in the community. Although there were early studies citing that tolerance to therapeutic effects of antihistamines could occur, more recent data, especially studies involving nonsedating antihistamines, indicate that tolerance to the therapeutic effects of these drugs does not occur.

Overall, it seems like the mechanism driving the sedation vs. the therapeutic effects are two separate down stream effects of regulating the inflammatory response. Neuronal tolerance and synaptic transformation is a fairly fluid and ongoing process, whereas the inflammatory response is much more robust. Meaning, the neuronal response is, theoretically, more able to adapt to chronic use of the anihistmaine while still giving the therapeutic effect. This hypothesis is supported by data, but yet to be confirmed, thus creating polarization on the topic.

Also see, Goodman and Gillman Pharmacological Principles of Therapeutics


Why do most theories assume "only" sexual reproduction can cause genetic diversity?

This is a pretty big question so I'm going to focus on the core points.

It's not nearly so either-or, and really a range of two things: trait diversity and stability. Sheer diversity isn't sufficient to improve rate of adaptation. Stability in the sense that it's a good idea to hold on to successful traits.

In sexual reproduction, you have two sets (one set of traits from each parent) of proven survivable traits to draw from. Very roughly, it doubles the amount of positive feedback toward maximizing fitness for the environment the pair finds themselves in - of which pathogens are a major and quickly changing component.

In asexual reproduction, you have a single tested set of traits. Asexually reproducing organisms thus depend on things like horizontal gene transfer - proven traits from another organism. This has the effect of prolonging the amount of testing that takes place (one organism vs two), causing asexual organisms to be more adaptable to the circumstances they find themselves in compared to sexually reproducing organisms and vice versa.

Where I have written "proven" here, I am referring to the fact that the traits in question have survived in combination with the organism's other traits, as opposed to a totally new mutation that could have consequences before the organism has a chance to reproduce.

Related literature

Genetic variation in organisms with sexual and asexual reproduction
"With realistic environmental changes small alterations in any particular measurement or trait are usually sufficient to keep up with the changes, but fitness, since it depends on a large number of traits, will be selected with greater intensity, which may be enough to confer a distinct advantage on sexual reproduction." An advantage of sexual reproduction in a rapidly changing environment.
Bacterial adaptation to pathogens: What antimicrobial resistance has taught us about horizontal gene transfer.


How is it that the WI-38 cell line isolated by Hayflick in 1962 is still very much around and not affected by the 'Hayflick Limit'?

The answer is that the majority of the cells were frozen from very early in their Hayflick lifetimes e.g. after 9 population doublings. They have been thawed out judiciously and only as needed thus preserving a lot of frozen stocks.  When an ampule of cells frozen at, for instance 9 population doubling, is thawed, the cells pick up where they left off and still have 41 doubling a to go.  So the magic of exponential growth combined with the fact that they keep dividing after being thawed has made for a decades- long supply . Does this answer the question to your satisfaction?


Short answer. It was discovered pretty early (late 1800's). It is easy to get (you probably know where it comes from), purify, grow and is not virulent. E.coli spreads very rapidly (30 minutes division rate).

Why this one in particular and not another similar bacteria? Well you have to choose something at some stage and usually the more an organism is used the most valuable it becomes which means that more and more scientists will start to use it creating a loop which favors certain organisms, like it happened with E.coli.

E.coli started to be studied because Theodor Escherich wanted to prove the "germ theory of disease" which led him and later other scientists to work with E.coli and everybody uses it today.

By the way, the mouse model is actually quite interesting. Started by breeding huge amount of mice for selling them as pets.


Is there any research on wolf and bobcat interactions?

In Sweden, no clear evidence have been found for interactions between wolf and European bobcat (Lynx lynx), see Wikenros et al, 2010. There, they have studied effects of wolfs on the survival of Lynx kittens, spatial movement of Lynx and Lynx' homerange size. The study finds no significant difference in any factor with/without wolves. They also speculate that the reason for a lack of interactions is that the two species use quite different main food resources (at least in Scadinavia); Lynx being specialized on Roe deer and wolves having wider preferences, but mostly Moose.

You should also look at the report Meta-analysis  on  the  effect  of  competition  between  lynx  and wolf on their diets (Lelieveld, 2013 which might provide more information. From reading the abstract, the report indicates no effects on wolves but that Lynxs might change their foraging behavior.


Can we use the HIV antibody test to detect HIV in newborns?

The rapid screen usually tests the oral mucosa by swabing the inside of the cheek and checking for the presence of anti-HIV envelope antibodies. Although the precise target of these antibodies seems to be kept propriatary, my guess would be the detection of either p24 antibodies or envelope antibodies that bind the V3 region.

Regardless, the point is they test for the presence of antibodies, which a child does not start making until they are born. See this post for a great explanation

Since a child has mostly maternal antibodies, the presence of anti-HIV antibodies would only mean that the mother has started producing antibodies to HIV (Seroconversion). This means that although the child has been exposed, they may themselves not be infected.

The mucosa, particularly in the oral region has a very low titer of anti-HIV antibodies, so I think this test would probably be best to direct the physician to conduct additional tests that are more indicative of HIV infection like p24 western blot.


Is the suicide of a moribund individual to be considered group selection?

It depends on what form of group selection you are talking about.
Group selection carries a lot of baggage and can refer to two very distinct concepts.  Concepts of group selection comes in two forms type 1, selection occurring on the group level, and type 2 selection on the group level that produces adaptations in said group or organism. The latter is the traditional usage of "group selection" the first(type 1) is now commonly (and confusingly) referred to as multi-level selection. (type 1 and type 2 are my terms I am using them to keep the two concepts identifiable)
Type 2 aka multi-level selection
Group selection (type 2) is simply selective pressures that occur above the individual level, kin selection could be seen as a form of this or it could not. It is still producing advantages and disadvantages to the genes and genes are still acting as the basic unit of evolution. Selection is occurring between groups with the differences between the groups being a product of the genes of the individuals within those groups. The genes are still favored or unfavored there is just many levels on which that the genes products can manifest. This models of group selection are basically just another form of gene based selection and adaptation it just adds another layer in which selection can occur.
Now few argue this form of group selection could not occur just that it would be swamped by normal gene based selection in most instances. There are genes known that are horribly detrimental to the individual and population in return for greatly favoring their own spread, the famous R2D2 gene in mice is an example.
Bacteria can be problematic in this as relatedness may not be a good measure of whether they share the same genes, and kin selection only requires shared genes. Could the behavior in bacteria be group selection in this case, yes, of course it could also be kin selection, the relatedness (Hamilton's original description) description of kin selection is really only useful in animals. In organisms with more lateral gene transfer they only need to share the gene in question, they could be completely unrelated in any other way. Indeed the paper even proposes this low but non-zero relatedness.
Now the big problem type 1
Type 1 is the traditional and first usage of the term group selection, but also the one only rarely proposed today, making it a very confusing term.
the big difference between kin selection and group selection (type 1) is that kin selection (or any form of selection including type 2) is about the selective advantage to the gene, an already well established principle, while many forms of group selection (type 1) propose a new "thing" on which selection occurs. what this thing is is never well defined but then neither were genes when natural selection was discovered.
To prove this form group selection and not kin selection you would have to show no selective advantage (or disadvantage) to the gene, basically you have to eliminate kin selection and other phenotypical expressions as a possibility. Proposed forms of group selection (type 2) can be shown to be products of normal gene based selection so you have to show this is not occurring. (thanks to Remi for this source). Intentional group formation in intelligent organisms (humans) is so far the only proposed mechanism in which this could work, and this would fall under memetics, which means it is occurring when related genetic differences are minor or non-existent.
Your paper does not show this form of selection, it does not even attempt to.
for a further breakdown of the diffrent forms of group selection I recommend this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850877/


What is the proper pronounciation of the scientific name of the ground elder / Aegopodium podagraria?

Here is a american database which offers sound samples for a lot of scientific plant names.


Species Identification: Beetle having trunk!

This is a weevil called Cleonis japonica. Here is a link to a specimen which was collected in 1904. (http://weevil.info/sites/weevil.info/files/Cleonis_japonica.jpg)
Here is a link to same site and one other which show where it was found.
(http://weevil.info/content/cleonis) and (https://www.iso.org/obp/ui/#search)
NP means nepal. Here is a link to something which I hope is a little more descriptive.

https://www.zin.ru/Animalia/Coleoptera/pdf/arzanov_grebennikov_2017_cleonini.pdf

I wish you had taken better pictures.


Identifying flying insect from southern Poland / Upper Silesia area

Found it, with a lot of help from my local neighbors. It is Melolontha melolontha or cockchafer.

From English Wikipedia:

The cockchafer, colloquially called May bug or doodlebug is a European beetle of the genus Melolontha, in the family Scarabaeidae.
Once abundant throughout Europe and a major pest in the periodical years of "mass flight", it had been nearly eradicated in the middle of the 20th century through extensive use of pesticides and has even been locally exterminated in many regions. However, since an increase in regulation of pest control beginning in the 1980s, its numbers have started to grow again.

Here, where I spotted this insect (Upper Silesia) it is called in local language (in Silesian language) "julik", which is quite correct, since they seems to appear in July.
However, as per above cited part and as per Polish counterpart to above cited article, officially this insect is called after May, either "May bug" (English) or "Chrabąszcz majowy" (Polish). Most likely because adult forms of this species appears mature by the end of April and through May.


Difference between pulse coupling and diffusive coupling In biological oscillators

Partial answer:

As for a book on the topic of mathematical modeling of coupled neural oscillators, you can start with:

Wilson, H. R. (1999) Spikes, Decisions & Actions: Dynamical Foundations of Neuroscience, Oxford University Press, Oxford UK. author's copy, amz


Who and when was the first human diagnosed with hemophilia, or considered a carrier?

The disease hemophilia has been known for much longer than that. At the time the Talmud was written, for example, it was known that if some boys in a family died from circumcision, the next were also at risk. This might have been because physicians recognized an inherited blood disorder.

Abulcasis, an Arab physicians of the 10th century, wrote about families in which male members died from bleeding out after injury.

In 1803, John Conrad Otto wrote about

  a hemorrhagic disposition existing in certain familie

Tracing the condition back three generations in that family named Smith, who lived in  Plymouth, New Hampshire. So there were definitely earlier cases where we even know the names of the patients, eben before the disease was named.

The word haemorrhaphilia, later shortened to hemophilia was first used in 1828 by Friedrich Hopff, before the birth of Queen Victoria.

Queen Victoria herself did not have the disease, though, she was a carrier. At least one of her sons had the disease and at least one of her daughters was also a carrier.

The history of hemophilia

History of Bleeding Disorders


Do seeds use cellular respiration when they are germinating?

Those stored fats and sugars have to be burned to be utilized. Besides how ridiculous it would be to have a multicellular organism mature using only fermentation.


Why Do we close our eyes while sneezing?

Mythbusters did this one!

The simplest response is that your eyes close as a reflex, because the nose and eyes are linked by cranial nerves which brings the sneeze signal to the brain and then to the eyes, making them blink. Would you eyes pop out if you managed to sneeze with them open? (a common urban myth) No! Your eyes are attached by strong muscles and it would take a lot more force than a simple sneeze to lose them.

Mythbusters article on the subject

I would love to give you a more scholarly article but this is the same one referenced on wikipedia on the subject, plus it's hard to find academia in the fluffiness of this question.


How can we create a living dinosaur using DNA technology?

It is widely accepted that birds are in fact dinosaurs. Cladistically speaking, no DNA technology is required to create a living dinosaur, as they already exist.

Assuming you want to do the same to a non-avian dinosaur (a paraphyletic group), however, a better idea would be to ask on World Building SE, as there have been little to no scientific research on the topic, and speculative answers are generally considered off topic here.


Why do more complex DNA strands take longer to anneal?

What is meant by complexity?
This is the crux of the matter. As is often the case, confusion arises from not defining one’s terms. In this case the three possibilities we have to deal with are:

The extent to which a sequence is not homogenous. e.g. ATATATAT is more complex than AAAAAAAA; ATGCATGC is more complex than ATATATAT; ATGCTCAG is more complex than ATGCATGC. This would seem to be the definition assumed by the questioner (and also in another answer).
The length of the sequence. This is the definition given in the article quoted in the question: “Complexity - the total length of different sequences”. However it is not one that would have occurred to me on encountering the expression.
The extent to which a length of DNA (especially a chromosome) has regions present in multiple copies. This seems not to have been considered in the question, but is historically what was meant be genome complexity deduced from annealing experiments. This is shown in these extracts from a venerable text on nucleic acids, long out of print:

In human cells unique DNA has a Cot1/2 value of 1000 (moles nucleotide seconds litre–1)…Repetitive DNA includes all of the rest of the DNA. Among the repetitive DNA is a fraction which reanneals with a Cot1/2 value of between 100 and 1000…thought to be those [genes] coding for proteins which form major structural components of the cell… [some examples given of multi-copy genes like tRNA]…At the other extreme DNA with a Cot1/2 value as low as 10–3 consists largely of satellite DNA.

Explanation for Case 3 (complex because of multiple copies)
As the article quoted in the question correctly states, “Renaturation, or duplex formation requires random collisions between two single-stranded molecules”. However such experiments are performed with fragmented DNA in solution, not whole chromosomes, so the two molecules that must collide are gene-size or smaller in length. The more copies of geneX or sequenceX there are in the DNA, the greater the number of targets there will be containing geneX or sequenceX, hence the faster fragments containing such genes will anneal.
Explanation for Case 1 (complex because less homogeneous)
Assuming that one is comparing single-copy genes of different degrees of homogeneity, one can imagine that for something like ATATATAT there will be more ‘hits’ that give partial overlaps that may be detected as double-stranded:
A T A T A T A T A T A T A T A T
        T A T A T A T A T A T A T A T A

Alternatively, once bound imperfectly, there may be a greater chance of perfect binding after dissociation because of proximity.
However, it is also possible that writers are confusing or amalgamating this with Case 3, as simpler DNA may actually be present in more copies in a genome.
Explanation for Case 2 (complex because longer)
The explanation here is trivial. If you perform reannealing experiments with two geneomes — E.coli (4.6 Mbp, c. 4000 protein-coding genes) and Carsonella ruddii (0.16 Mbp, 182 protein-coding genes) — employing the same amounts of DNA as 300bp fragments, the fragments from the smaller genome will be approximately 20x more likely to make a random collision with a complementary fragment.


How is cancer associated with host pathogen interaction?

No not necessarily. Cancer can also be caused by bacteria and viruses in your body

The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored.
Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses.

You can read more here: Aituov, Bauyrzhan, et al. "Pathogen-driven gastrointestinal cancers: Time for a change in treatment paradigm." Infectious agents and cancer 7.1 (2012): 18.


That's not a typo. The author is talking about cooking polysaccharides (gelatinisation), which in fact increases the digestibility:

  Gelatinization refers to the irreversible loss of the crystalline regions in starch granules that occur upon heating in the presence of water. The temperature range during which the crystalline structure of the starch granule is lost is dependent on the water content, and on the type of starch. The gelatinization dramatically increases the availability of starch for digestion by amylolytic enzymes. (emphases mine)

Source: FAO: Effects of Food Processing on Dietary Carbohydrates.

You can read more about it in this Wikipedia page.


Does evolution go only in one direction?

No, it does not. There is no such thing as a goal of evolution at making things fly or at making things intelligent or whatever. There is no intrinsic directionality.

In short the reasons are 1) Evolution is much more than just natural selection 2) natural selection does not systematically select for a specific trait. Some traits are advantageous under some ocnditions, some other traits are advantageous under other conditions.

I won't talk more about the mechanisms of evolution here as it would take a whole book. Instead I will recommend a source of information for you to further your knowledge.

Source of information

As your question is very introductory and shows misunderstanding, you might want to have a look at an intro course to evolutionary biology such as for example Evo101 by UC Berkeley.

Devolution

Note that this term is rarely used in the scientific literature (actually I think I have never encountered it in the scientific literature). From wikipedia:

  In modern biology the term [devolution] is meaningless: evolutionary science deals with selection or adaptation that results in populations of organisms genetically different from their ancestral forms, where evolution has no intrinsic directionality. The discipline makes no general distinction between changes leading to populations of forms less complex or more complex than their ancestors, and in such terms the concept of a primitive species cannot be defined.

The question is a bit unclear

There is a slight issue with the question as it is not that easy to categorize all animals as living strictly in the water, on land or in the sky. Note that almost no living things live strictly in the sky without ever touching the ground. Here are a few examples of limit cases

oysters
dragonflies (larvea live in the water, adult fly)
flying squirrels
Most ducks (spend much time on water but nest on land)

As a consequence the question is very undefined

Examples of potential interest to you

The question is undefined but here are a few examples of cases anyway that will interest you. For simplicity, I will reduce my list to animals only and will not consider similar cases in procaryotes, and non-animal eukaryotes such as plants and fungi.

Whose ancestors were terrestrial

Cetacea (blue whale, orca, dolphins, ...)
Sirenia (dugong and manatees)
Pinnipeds (sea lions, sea leopards, ...)
Monotremes
Marine iguana (and other swimming lizards)
Beavers
Otters

Whose ancestors were flying

Penguins
ratites (Ostrich, emu, kiwi, ...)
dodo
Many birds are able to stay for relatively long period under water when hunting for fish.
Ants and other non-flying hymenopterans.
Ground beetles and other non-flying beetles
water beetle

Again, categorization is not that easy. I just want to highlight the water beetle as example where the ancestor was marine, then terrestrial, then flying, then non-flying and finally living in the water again.

Related post

How many times did terrestrial life emerge from the ocean?


What came first? The DNA or the DNA polymerases?

The straight forward answer is: we don't know. We don't have any direct evidence for what happened at that time nor any completely developed and coherent theories for how it worked.

The widely believed hypothesis is the "RNA World" hypothesis. RNA, unlike DNA, is capable of spontaneously folding to form catalytic molecules and thus avoids the needs for translation and transcription by proteins since it can bootstrap it's own synthesis. The idea is that, over time, the RNA developed the means to synthesize proteins and then started using DNA as a more stable storage molecule. The earlier RNA-based RNA polymerases were supplanted by higher fidelity protein polymerases over evolutionary time so we no longer see them in modern cells.


I doubt you'll get a positive ID from that photo. It might be some woodboring beetle, maybe genus Anobium or Hedobia. FTR, if they are chewing on your wooden floors, you might be able to hear them if you listen carefully.
I suggest you collect some, maybe even living, in a small tube and ask a specialist. My first idea would be someone at a nearby university or natural history museum working in entomology, and specifically on Coleoptera if possible.


Darwin's first sketch of a phylogenetic tree

This is from Darwin's Notebook B: Transmutation of species from 1837–1838. From what I understand, the tree is a hypothetical depiction of descent used to discuss differences and relatedness between forms/species. This is the text that accompanies and follows the sketch (notebook pages 36-44):

  I think
   (sketch)

  Case must be that one generation then should be as many living as now. To do this & to have many species in same genus (as is) requires extinction.
  Thus between A & B immense gap of relation. C & B the finest gradation, B & D rather greater distinction. Thus genera would be formed. — bearing relation

  (page 37)

  to ancient types. — with several extinct forms
  for if each species an ancient (1) is capable of making 13 recent forms, twelve of the contemporarys must have left no offspring at all, so as to keep number of species constant. —
  With respect to extinction we can easy see that variety of ostrich, Petise may not be well adapted, and thus perish out, or on other hand like Orpheus being favourable

  (page 38)

  many might be produced. — This requires principle that the permanent varieties produced by inter confined breeding & changing circumstances are continued & produced according to the adaptation of such circumstances, & therefore that death of species is a consequence (contrary to what would appear from America)

  (page 39)

  of non-adaptation of circumstances. —
  Vide two, pages back.
  Diagram
  The largeness of present genera renders it probable that the many contemporary, would have left scarcely any types of their existence in the present world. — or we may suppose only each species in each generation only breeds; like individuals in a country not rapidly increasing. —

  (page 40)

  If we thus go very far back to look to the source of the Mammalian type of organization; it is extremely improbable that any of his relatives shall likewise the successors of his relations shall now exist — In same manner, if we take a man from any large family of 12 brothers & sisters in a state which does not increase

  (page 41)

  it will be chances against any one of them having progeny living ten thousand years hence; because at present day many are relatives, so that by tracing back the descen fathers would be reduced to small percentage. — & in therefore the chances are excessively great against any two of the 12. having progeny after that distant period. —

  (page 42)

  Hence if this is true, that the greater the groups the greater the gaps (or solutions of continuous structure) between them. — for instance, there would be great gap between birds and mammalia, Still greater between

  (page 43)

  Vertebrate and Articulata, still greater between animals & Plants.
  But yet, besides affinities from three elements, from the infinite variations, & all coming from one stock & obeying one law, they may approach, — some birds may approach animals, & some of the vertebrates invertebrates —
  Such a few on each side will yet present some anomaly & the g bearing

  (page 44)

  stamp of some great main type, & the gradation will be sudden.
  Heaven know whether this agrees with Nature: Cuidado.

The text together with actual pictures of the notebook pages can be seen at http://darwin-online.org.uk. Pages ~38-41 are often seen as key ideas for Darwin's formulation of natural selection. Also note that the presence/absence of a horizontal line at the tips are apparently used to denote extant vs extinct groups (see notes in link above).


Which DNA elements belong to the definition of a gene?

Usually a promoter is not considered a part of the gene. Distal regulatory elements qualify even lower for being considered a part of a gene because they can regulate many genes simultaneously.

Basically, a geneic region starts from the transcription start site (TSS) and ends at the terminator (or polyadenylation/cleavage site in eukaryotes). If a gene gives rise to multiple transcripts, those which have similar products (no frameshifts) but different TSS/terminators, we should consider the geneic region as a union of all the primary transcripts produced from that site.

There is a relatively old article on this topic: What is a gene, pose ENCODE? History and updated definition. It summarizes that:

  There are three aspects to the definition that we will list below,
  before providing the succinct definition:

  A gene is a genomic sequence (DNA or RNA) directly encoding
  functional product molecules, either RNA or protein.
  In the case that there are several functional products sharing
  overlapping regions, one takes the union of all overlapping genomic
  sequences coding for them.
  This union must be coherent—i.e., done separately for final protein
  and RNA products—but does not require that all products necessarily
  share a common subsequence.

  This can be concisely summarized as:

  The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products.

.

My summary is that a gene, if it codes for a protein, would be a union of all primary transcripts that produce identical proteins (originating from transcripts with different TSS/terminators) or splice variants.
Ideally, all the different transcripts produced from the locus would have the same promoter.

Overall, it appears that a common promoter is imperative for considering the different products under the same gene because if two products are produced from different promoters then we consider them as products of overlapping genes.

Whether we should consider the promoter as a part of a gene is an open debate.


Cancer: what does it mean "at presentation"?

"Presentation" is the event where the patient first visits the doctor.
For example, "the patient presented with yellowing skin and complaining of abdominal pain".
The paragraph you have doesn't make this clear, they assume you have already had your genome sequenced prior to visiting the doctor, who looks at the result, uses this tool and predicts what is likely to happen to you and your cancer based on your DNA.


How do Kangaroo mothers deliver the correct kind of milk to the correct joey?

The younger Joey remains attached to the teat from which it receives its milk for the period of nine months until it leaves the pouch. So that would be teat from which milk suitable for the newborn is available (reference 1 and reference 2). The older Joeys also have an incredible sense of smell by which it can detect the teat from which it gets the milk it requires but it stands to reason that they cant get milk from the teat to which the younger joey is attached. (reference)