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What is the effect of self envenomation on reptiles?
If a venomous lizard bites its own tongue will it die?
I've searched the whole internet and I am unable to find a reliable answer on self envenomation.

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Sounds like a fun experiment

TL;DR
No, it won't die. Lizards/snakes are usually immune to their own venom.
Since I couldn't find a good answer to this recurring question on this site, I will try to summarize it here. I found more research on snakes than on lizards, but for now we will just assume that similar mechanisms can be found in lizards.
First, the question is how the venom kills the prey. What does it do in the body?
A common mechanism is a block of acetylcholine receptors at the neuromuscular junction. Simplified, these receptors activate muscle contraction upon a neuronal signal. When the receptor is blocked by the toxin, the neuronal signal cannot be transmitted to the muscle, which paralyzes the animal. Research has shown, that some snakes and lizards have evolved different acetylcholine receptors, that can still bind acetylcholine (and activate muscles), but not the toxins (source1, source2). This makes them immune to the most common neurotoxins found in reptile venom.
Another mechanism is hemorrhagic activity of the toxin, which is a disruption of blood vessel integrity resulting in bleeding and death. This was linked to a proteolytic ("destroying proteins") function of venom compounds (source3, source4, source5). The blood serum of snakes can contain factors that block the hemorrhagic function of toxins, possibly by neutralizing the mode of action (inhibiting proteases). This could be specific antibodies/inhibitors or an adaptation of serum proteins (source6, source7, source8).
Further research has implicated phospholipidases (destroying phospholipids like used in cellular membranes) as the mode of action for snake venoms. Again, phospholipidase inhibitors can be found in the blood serum of the snakes themselves. There were also reports, that the expression of these inhibitors changes from younger to older snakes (source9, source10) and can be induced by venom injection (source11). It is therefore hypothesized that venomous snakes or lizards are repeatedly exposed to small amounts of their own venom, building up immunity over their life span.
Other modes of action include myotoxicity (destroying muscles), edema-formation or blood thinning. Again, it depends on the specific mechanism and how snakes and lizards have adapted to be immune to these.
Since similar toxins are found in several species, snakes and lizards are often not only immune to their own venom, but also to bites of other members of the same species or other related species.


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How to find the enhancer region of a specific gene?
I am new to these concepts in biology and need some help understanding. My main concern is how to find the enhancer of my gene of interest, specifically the sequence of the enhancer. I am working on a project where I will be attempting to use CRISPR- mediated deletion of the promoter region and enhancer region in my gene of interest FOXN2, in MCF7 Tamoxifen resistant breast cancer cells. I already have the sequence for the promoter region from UCSC's GenomeBrowser, but I'm not sure if the enhancer region sequence can just be looked up on there or anywhere else. Do I need to do a protocol to find the enhancer region myself? I have seen many things about ChIP-Seq and that I may need to do that to get data to find my enhancer but I am just not sure. I plan to use the sequences of the enhancer and promoter region of my gene of interest to create gRNA for CRISPR. Thank you to anyone who can help.

Encode is a good resource for browsing cis-regulatory elements in the human and mouse genomes.  Here is the page listing candidate cis-regulatory elements proximal to the human FOXN2 gene.

Remember that genes can have several enhancer and repressor regions and they can be spread more or less all over the genome if you're unlucky. FOXN2 seems to be reasonably well-known though, so there should be information on this out there.

There are several ways to identify enhancers:
(1) Chip seq / chip-chip recognize transcription factor binding sites,
(2) Enhancer specific factors can also be used to identify enhancers, such as EP300, the binding sites of EP300 are often used to predict enhancers;
(3) RNA polymerase II can bind thousands of enhancers, so POLR2A2a, the largest subunit of RNA polymerase II, can also be used to search for enhancer sites;
(4) The high sensitive site of deoxyribonuclease I (DHS) represents the open chromatin region, many of which are covered with enhancers;
(5) A large number of active regulatory elements, including enhancers, can be identified by formaldehyde assisted separation regulatory elements (face) combined with sequencing;
(6) Some histone modification patterns reflect different chromatin states, such as the binding of h3k4me1 and h3k27ac, which are widely used for enhancer labeling;
(7) Enhancer sequence can be transcribed, and the transcriptional enhancer RNA (enrna) is also a marker of enhancer activation;
(8) The method of chromosome 3D conformation (e.g. 5C and Chia pet, capture-c) can also provide the information of enhancer promoter interaction.

Welcome and thanks for your interesting contribution. Can you add some sources to your answer, preferably references to journal papers? But also a wiki link here and there can help other users a lot to background read on your material. Cheers.

source: Stack Exchange

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

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What percentage of RNA splicing happens during transcription?
Splicing can happen either during transcription, or directly afterwards.
I am reading about single-cell RNA seq, and according to this paper, they observed that 15–25% of reads contained unspliced intronic sequences.
Now assuming that the majority of reads from RNA seq will come from RNA that has finished being transcribed...
Does this suggest that 75-85% of all genes are spliced during transcription? In other words, are 80% of our genes fully mature (spliced) immediately following transcription?

I don't think it will be possible to give a conclusive answer to this question, because a) it's a matter of active research and b) the rate / percentage of transcripts that are fully spliced co-transcriptionaly is almost certainly not constant but will depend on a lot of factors & regulatory mechanisms.
Another important detail is that this analysis / paper is based on mRNA sequencing, which uses oligo-dT primers to enrich for polyadenylated mRNA molecules. However, oligo-dT primers can also bind to stretches of A's inside of RNA molecules (this process is called internal priming) and since such stretches are more common in introns compared to exons this may contribute to the abundance of intronic reads in mRNA sequencing data (I don't have a good literature source for this specific case, but it's a known 'issue' for sure).
Maybe some of these reviews are also helpful (not sure if all are freely available):

Splicing and transcription rates in living cells
Environmental influences on RNA processing
Co-transcriptional spliceosome assembly and function

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


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Curious on the species of a large Orange Spider?
Heres the images of her:

She just laid a large yellow fuzzy sack of babies recently (Were pretty sure were just going to deposit her and her eggs in a grove in the forest soon)
We have lots of brown recluses here in North Carolina, but no idea what she is.
Climate: Humid, Tropical.
Zone: Sneads Ferry, North Carolina, United States.
Size: About 1.5 Inch, leg spans are about 1 inch on their own.

Related: Spider Identification Illinois


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Changes in dna from dioxin poisoning
A person sprayed with a dioxin, how long would it take for a dna change? Instant or over time? Would that person having children afterwards pass on any(if any) dna changes?

Studies on model organisms suggest effects begin quickly, within 6-8 hours of exposure. Rat studies suggest liver absorption of dioxin reaches a maximum from 8-24 hours, with Cytochrome P450 protein expression levels peaking afterwards. Another study uses a comet assay that measures DNA damage after six hours of dosing, and damage is tied to dose level.
Epigenetic changes to sperm and eggs are heritable, passed along to offspring. These result from histone deacetylation and methylation, which in turn change how DNA are packed and unpackaged for protein expression, and change expression itself.
A summary article on epigenetic dioxin (TCDD) toxicity suggests that there are specific effects on protein expression involved in embryonic development in model organisms, which result in birth defects and immune system damage.
In addition to controlled lab experiments on rats and mice, the United States of America and Monsanto conducted a massive, uncontrolled science experiment on humans, dropping dioxin in great quantities on millions of Vietnamese civilians during the Vietnam War.
Children of exposed victims suffered spinal bifida and other birth defects. US military exposed to dioxin in the course of deploying this chemical weapon also had their children suffer greater rates of similar birth defects.

Awsome,  thank you for the information... also does anyone know what immune changes with dixon poisoning?  Thank you in advance...


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Why does the cervical vertebrae contain more white matter than the more lower parts of the spinal cord?
Why does the cervical vertebrae contain more white matter than the more lower parts of the spinal cord, like the lumar vertebrae?
In white matter are the axons of interneurons.
Anyone know this?

This is true according to my book, but why?

Try thinking about where those axons are going and where they are coming from, does that help?

They signals come from the receptors and go to the brain and then they get back to the muscles/glands. But I dont see why you would need more axons around your neck, instead of your trunk, because thats where most body parts are.

Try drawing a simple diagram where you connect the brain to muscles in the body with wires, and in another color from the peripheral receptors to the brain, and see what it looks like.

Btw I am Dutch. Peripheral means in the non-central nerve system right?

Yes - for this exercise it doesn't really matter though. You will get the same answer even if you just draw the axons going to muscles.

Still dont get it, could you just give the reason?

The neck part has more receptors?

I think I know it: there is more white matter upwards because there all the axons meet up, causing it to be more white, due to myelinated cells of Schwann?

Yep, pretty much. There are more axons in the neck because it has to contain all the fibers from all the rest of the body heading to the brain. Axons in the spinal cord make up "white matter" because they are mostly myelinated, and myelin is white. Since you've figured it out you could write it up as an answer and answer your own question here.

There is more white matter upwards because there all the axons meet up, causing it to be more white, due to myelinated cells of Schwann.

Welcome to Biology.SE! I'm sorry you're not receiving a more positive response to your first posts, but I encourage you to persevere — as a first step please take the [tour] and then consult the help pages for additional advice on [Answer] and [Ask] questions effectively on this site. ——— Specifically, this answer sounds reasonable, but it is much more likely to receive a favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). Thanks!


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Analysis of post transplantation lineage tags
I'm having some trouble understanding some bits of a study, mostly about the Sleeping Beauty system and TARIS model, from this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4408613/
I understand the concept, but not how it works technically. Can anyone explain it for me?

I can't find a reference to a "TARIS model" in the paper you linked, but we can break down the molecular circuitry of this lineage tag tracking system step-by-step.

The authors use a type of Tet expression system in order to tightly control the expression of a hyperactive Sleeping Beauty (HSB) transposase.  In the absence of doxycycline, the reverse tetracycline-controlled transactivator M2-rtTA does not bind the TetO operator. Jackson Labs has a very good summary of Tet-On (and Tet-Off) systems:

... rtTA is a fusion protein comprised of the TetR repressor and the VP16 transactivation domain; however, a four amino acid change in the tetR DNA binding moiety alters rtTA's binding characteristics such that it can only recognize the tetO sequences in the [tetracycline-responsive promoter element (TRE)] of the target transgene in the presence of the Dox effector. Thus, in the Tet-On system, transcription of the TRE-regulated target gene is stimulated by rtTA only in the presence of Dox.

In the presence of doxycycline, the transactivator drives expression of HSB from the constituent promoters of the TetO operator.  HSB contains DNA binding motifs that specifically recognize the direct repeats (white triangles) and a catalytic domain that excises the direct repeats and the DNA they flank, which contains a transcription stop signal (Tn-STOP).
Excision of the Tn-STOP signal allows for expression of DsRed driven by a strong synthetic promoter (CAGGS, first described here).  The excised sequence is then inserted somewhere else in the genome.
Because successful Tn-STOP excision is concurrent with transcription of DsRed, red fluorescing cells can be selected and prepared for NGS.  HSB transposition is "random", so two different transposition events are unlikely to target the same insertion locus.  The specific insertion site can then be used as a molecular fingerprint to identify the progenitor stem cell after replication and differentiation.


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Is there a definition of species where Lions and Tigers are the same species?
According to Species concepts

There are at least 26 recognized species concepts

And according to Why are lions and tigers considered different species (not sure how reliable this source is though, but I've seen exactly the same answer in another website)

The reason tigers and lions are different species is because of different behaviours, different habitats, different social hierarchies, and they each have their own subset of genes that they share within their species (like the genes for stripped fur or for manes).

Now, I'm not sure about "social hierarchies" (which I'm sure it's a fuzzy concept) , but there are different breeds of dogs with different behaviors, living in different habitats, and there has to be differences in genes in different breeds, since even in humans populations there are 1% of differences in genes and according to other sources more.  Then my question is, since Tigers and Lions are closed to each other to the point they can produce offsprings, is there any of those 26 definitions of species where lions and tigers are the same species?

The concept this would fit under would be the "Biological Species Concept."
Concerning this concept, the Evolution site for Berkeley says "members of populations that actually or potentially interbreed in nature..." constitute a species. By this definition, since lions and tigers can (and do) interbreed, they would be considered the same species under this concept.
EDIT: As Bryan pointed out, though, lions and tigers do not breed outside of captivity. NatGeo and Britannica both second this. With this, then, the Biological Species Concept would not be viable.
EDIT2: With the above in mind, there don’t seem to be many options.
Mate-Recognition: This idea posits that organisms who “recognize one another as potential mates” (Wikipedia, “Species”) make up a species. By this, it could be argued lions and tigers are the same species, but I would be hesitant for this to be the concept, for the same reasons against the Biological Species Concept (not occurring in nature).
Ecological: Using this definition, a species is made up “of organisms adapted to a particular... niche, in the environment” (Wikipedia). Again, this is very fuzzy, as I wouldn’t define them in the same niche (though this might depend on how specific you get).
Conclusion: These seem to be the most likely, though that’s a very loose term. I couldn’t find any others that would fit nearly as well. I would say the answer is “no”, but I don’t think I found all of the concepts.

I think one could question this. Although lion-tiger hybrids are viable, occasions where those hybrids have been able to reproduce themselves are quite rare, and they can be effectively considered sterile. They also only interbreed in captivity.

@Bryan Good point. Thanks for that!

Your quote...

The reason tigers and lions are different species is because of different behaviours, different habitats, different social hierarchies...

...is not entirely correct: lions (Panthera leo) and tigers (Panthera tigris) overlaped geographically in the past, since Panthera leo was common from western Europe to southeastern Asia. On top of that, if you consider that Panthera atrox is actually Panthera leo (which is the view of some paleonthologists), you can even add America to the list.
Until today there are (very few) lions in India (photo: Wikipedia):

And, despite that geographic overlapping, lions and tigers do not breed, so we can clearly rule out Mayr's BSC.


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How do cis-regulatory elements and trans-regulatory elements behave differently?
Suppose you are working with an operon in a diploid organism.
I'm looking for either a biochemical or genetic explanation.
What I'm having trouble with mainly is understanding how something would only be able to regulate a gene on one chromosome but not the other. I was thinking cis would be favored because the gene is close by, but everything is just floating around randomly in the cell so it should favor cis either way and level out if you waited long enough.

Aside from "just floating around randomly", molecules also change the conformation of DNA and can move along the DNA. Such effects will propagate along the DNA and thus act in cis but not trans.

I was thinking cis would be favored because the gene is close by

Your intuition is correct.  Cis-regulatory elements like enhancers are more efficient at enhancing transcription of genes in cis than genes in trans, but trans interactions of cis-regulatory elements do occur.  Take a look at figure 2B of this paper and the accompanying text:

... quantitative RT-PCR showed that relative levels of GFP transcripts from constructs inserted at 37B were similar to those from transgenes at 53F, with 1.7% [95% C.I., 1.6–1.8%] of total GFP transcript in eye discs where GMR acts in trans relative to those where activation is in cis ...

The interaction of alleles between homologous chromosomes is called transvection, and this can be realized as binding of the enhancer associated with one allele to the promoter of the other allele.  Figure 9 of this paper is a good explanatory graphic.


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Are there solitary animals communicating with themselves?
I can imagine 3 different kinds of communication between individuals:

Communication between individuals of the same species.
Communication between an individual and another from a different species.
Communication between an individual and the same individual at a different time, i. e. some individual "taking notes" or "marks" for later use.

My question is whether there are animals showing (3) but not (1) or (2).
In order to make sure the absence of (1) I stipulate that the individual animal should be capable to live a completely solitary life, which excludes e. g. all mammals from the list of candidates.
Here, the criteria for "communication" are the following:

The message is created by a defined action of the animal.
The message is an object, separate from the animal's body.
The animal is able to interpret the message at a later time, i. e. removal or modification of the message artifact would result in a different behavior.

This question is motivated by the more general question whether the ability to communicate necessitates a social context.
EDIT: In order to make it clearer what communication could be, as suggested by the comments, here are a few examples:

territory marking: matches the categories (1), as a signal to rivals and probably (3), as a reminder for the territory owner.
alarm call: matches (1) and/or (2)
behaviour of the Honeyguides: a typical example of (2)
creation of trails: may have a communicative function (e. g. for ants), and is also seen with solitary animals. Is there a case, where the communicative function is predominant and all other criteria are met?

Here is why I think that some classes of species can be excluded:

mammals, birds: every individual enjoys parental care, which has a communicative aspect of type (1)
plants: may be able to communicate with other plants or animals, but self-communication seems hard to imagine.

I think this is an interesting thought, but almost certainly bound to lead to an inconclusive result relative to the motivating question. I think your (3) might be bound up too much in "language" and abstractions that are far higher order than communication more generally. If an animal recognizes a burrow as smelling "like home" and part of that scent includes smells originating from the individual animal, does that count as taking notes or marks?

There's also the problem of identifying a truly solitary animal; you've excluded mammals already, but even non-mammal animals that live alone find a mate, for example, and even animals that don't mate with a particular individual, like cnidarians, communicate with each other to coordinate gamete release. Even unicellular organisms communicate with one another, as do plants. Communication seems to be a much more generic feature of life than the premise in this question seems to recognize.

@BryanKrause I think the burrow smelling "like home" would meet the criteria (2) and (3) (if there is the observation), but perhaps not (1) unless the scent is applied by an act like spraying or so.
Please note also, that animals that do mate are not excluded, because that fact says nothing about a particular individual that might well live its life alone (I've tried to clarify this by an edit of the question).

It would be cool to have a brief beside the three common types, like "territory marking" "alarm call", it would make the question more accessible.


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How can I liquefy egg shell membrane
I want to extract egg shell membrane from the eggs.
And I want to put them together and turn them into fluid so that I can make whatever shape I want.
Is there any method that can make them into fluid?( like using acid or whatever)
+a egg shell membrane consist of collagen.

you need to edit your question,a large part of the membrane in eggs are made of keratin.source: https://www.exploratorium.edu/cooking/eggs/eggcomposition.html

some research is expected before posting.

If egg shell membrane really consists of collagen - here is your answer:
Cook it at 160 degrees Fahrenheit (=about 71 degrees Celsius) over a long period of time until it turns into a gel. I am pretty sure it will harden as soon as it is fully cooled down.
"collagen begins to melt at about 160F and turns to a rich liquid,gelatin"
"Denaturation of the collagen molecule is a kinetic process, and hence a function of both temperature and duration of heating. Cooking at low temperatures require long periods of time to liquify collagen."
Source: https://www.scienceofcooking.com/meat/slow_cooking1.htm


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Contrast Media for Plant cells
I currently have a waterweed (elodea) preparation for my optical microscope but i can only see some of the structures (membrane, wall, chloroplasts and the nucleus).
Now I want to see more (Like the Vacuole, Peroxisome, Mitochondria, Amyloplast, Ribosome, Golgi Apparatus, and endoplasmatic reticulum if possible with an optical microscope)
I know there are contrast media like the lugol's iodine solution (iodine-potassium iodide solution) but what will it show? And are there more?
Thanks in advance


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How does a drastic change to the genome persist and spread?
I just read the article on songbirds in the November, 2019 Scientific American. The article explains that songbirds have an extra chromosome, called GRC (germ-line restricted chromosome) that other bird species don't have, and there's a hypothesis that this may have been partially or wholly responsible for the diversity of this group of species.
The following line caught my attention:

Once the GRC originated in the last common ancestor of songbirds, members of that ancestral species that carried the GRC could produce fertile offsping only with mates that also had the GRC.

But when the mutation that created the GRC occurred, who did that bird mate with in the first place?
My belief is that most genetic changes are relatively minor, so they don't immediately result in incompatible mating. Speciation occurs as genetic changes accumulate over time. But the above quote implies that an entirely new chromosome is too drastic to allow interbreeding at all.
Wouldn't there need to be a whole bunch of birds who all had this extra chromosome at the same time to allow it to spread through the population? That seems unlikely to occur.
Am I just reading the line too literally? Could early birds with the extra chromosome mate with other birds, until the new chromosome accumulated too many changes?

It isn't necessarily true that individuals with different numbers of chromosomes are infertile. Even though common wisdom has it that horse (64 chromosomes)/donkey (62 chromosomes) hybrids are invariably infertile mules, that's not true; a significant number of fertile horse/donkey offspring have been documented.  Here is an example where the chromosomes were checked and confirmed to be 63 in the fertile mule parent.
Even more dramatically, the common shrew (a single species) has many different chromosome numbers as natural variability (at least 50 different chromosomal variants were identified in one paper) and this doesn't affect their interfertility.
So there are three general answers to the question here, though I don't know which is the most likely.

The extra chromosome arose and the original variant was very fortunate to have offspring; similar to the rare horse/donkey fertile hybrids.
The extra chromosome arose but had little effect on interfertility; similar to the common shrew. (The quote from the article in the question argues against this, but I don't know if it's a presumption made by the researchers, a presumption made by the writer, or a demonstrated fact.)
The extra chromosome arose in a single litter, so that several siblings shared it, and then interbred. Although incest avoidance is generally quite strong, animals that colonize islands or distance geographic areas (invasive species, often) commonly do interbreed this way.

When I was thinking about it myself, incest was one of the possibilities that came to mind.

The article seems to directly contradict your #2.

Not clear to me from your quote whether that's a presumption made by the researchers, a presumption made by the writer, or a demonstrated fact. In any case, I'll leave #2 in as a general possibility but will note that the article argues against it

Indeed, the article was written by a SciAm editor, not one of the researchers. So she may have been simplifying.

It seems like one of the rare cases in which the duplication of the specific chromosome  is not lethal, but actually advantageous. This means it can happen from time to time to see this extra chromosome by errors in cell-division.
Now although its unlikely, it eventually happened, that two birds with the same duplicated chromosome meet and mate: They replicate their "new species".
Note that the name of this "germ-line restricted chromosome" might be the cause of confusion! Any additional chromosome would be "germ-line restrictive": Unless all chromosomes are matched, cell-division is prevented by control mechanisms.
And some direct answers:

But when the mutation that created the GRC occurred, who did that bird
  mate with in the first place?

It needs to find a bird with the same additional chromosome!

My belief is that most genetic changes are relatively minor, so they
  don't immediately result in incompatible mating. Speciation occurs as
  genetic changes accumulate over time.

True, it takes considerable mutations for 2 chromosomes being unable to be paired, but here we speak of an additional chromosome: It intrinsically cannot be paired.

But the above quote implies that an entirely new chromosome is too
  drastic to allow interbreeding at all.

Exactly!

Wouldn't there need to be a whole bunch of birds who all had this
  extra chromosome at the same time to allow it to spread through the
  population? That seems unlikely to occur.

It takes 2 birds and coincidence!

Am I just reading the line too literally? Could early birds with the
  extra chromosome mate with other birds, until the new chromosome
  accumulated too many changes?

I don't think so!


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What is the fundamental difference between human genome and other genomes that makes human a self-conscious living organism?
DNA is considered to be the blueprint from which any organism can be created.
DNA carries the genetic information to construct a living body. DNA carries genes which represents the information that is used to produce proteins which operate and shape the body. So what exactly is the difference in human genome which sets it apart from other species
and makes it self-conscious ? Are there specific genes for self-consciousness that makes a particular animal conscious ?

I have edited your (naive) question, replacing your misuse of "genetic code". See the Wikipedia entry to get the answer to what the genetic code is. The secret of conciousness, you won't find an answer to.

DNA is considered to be the blueprint from which any organism can be
  created

It's the main blueprint, true, but in order for DNA to be functional it needs a complex composition of proteins, ions, membranes, sugars etc.. You know, all your cells have the same DNA, yet they all are different!
A friend of mine, a leading expert in stem cell manipulation, is even struggling to force a single differentiation of his stem-cells. So no, no one can create an organism solely from it's DNA.

So what exactly is the difference in human DNA which sets it apart
  from other species and makes it self-conscious ?

The building blocks of DNA, the 4 nucleotides, are the same for all living organisms.

Is there a specific gene for self-consciousness that makes a
  particular animal conscious ?

The interaction of genes is way to complex to point out a single most relevant gene responsible for consciousness. There is not a single gene that functions without the others. Anyways, the human brains function is heavily dependent on it's structure; the physical connection between cells. So if you want to search for genes that are involved in consciousness I would look at the group of structure/differentiation controlling genes. For example NOTCH2NL was found to be involved in control of the brain size. (The Notch protein family is involved in developmental differentiation and acts through cell-cell contact)

Biritsh Scientists have successfully created a new organism 'Syn61' from recoded genome. You can refer article published in Nature [https://www.nature.com/articles/s41586-019-1192-5.epdf]. So its possible to create an organism from its DNA.

@chaitanyabudkule: You've misunderstood that paper — they replaced the genome of a strain of E. coli with a synthetic version.  This would not work without the "machinery" (proteins, RNAs, membranes, metabolites etc.) present in the "host" bacterial cell.

While we likely do not know exactly what constitutes consciousness, we can likely surmise that other organisms are conscious (or at least show what we might call self-awareness), and we can probably agree that the brain (or at least a nervous system) is an organ critical to developing and maintaining consciousness in an organism. The Hox family of genes (and their associated DNA sequences) guide the orientation of embryonic cells and the subsequent development of the brain in most eukaryotes, including humans. Cites of relevance: 1) https://en.m.wikipedia.org/wiki/Hox_gene 2) https://www.ncbi.nlm.nih.gov/m/pubmed/20795329/ 3) https://en.m.wikipedia.org/wiki/Self-awareness#Animals

DNA may be the blueprint, but - like the blueprints used in construction - it does nothing without a whole bunch of complicated machinery, which we call a parent.

I don't know what your comment means, I'm sorry.

It means that if you have a string of DNA, it basically won't do anything unless it's imbedded in a cell.  And it has to be a cell of the proper sort.  Unless I've totally misunderstood biology, if you want to make a frog, you have to put the frog DNA in a frog egg cell.  If you put it in say a rat egg cell, I doubt if you'd get anything viable - though it might make an interesting experiment.  It'd be like handing the blueprints for an airplane to a housing construction crew :-)

I don't know what your comment means in the context of genomics or developmental biology, which is the crux of the question. If you have a better answer, please post it separately.

Nothing! If DNA is one way of doing life–which is not well defined–it has shown that in all its forms it has been creating organisms with some form of intelligence. If you can accept that there can be different levels of consciousness and intelligence, then it may almost be easier to ask which organisms have zero consciousness?
Here's a video showing that plants have intelligence in that they respond to current events and plan responses for the near future. Plants have their own kind of nervous system from Science Magazine.
Clearly, it must be like something to be a plant.

Are there specific genes for self-consciousness that makes a particular animal conscious ?

The mechanism of self-consciousness in the brain (in the cortex) is separate from the formation of the brain which is separate from the genetic control of the brain development. You want an answer for the genetic control of the brain development (cell differentiation, embryonic development) that will explain the mechanism of self-consciousness at the same time.
So; the short answer is "No, there are not".
It is clear that consciousness is the product of a brain structure which is made of complex connections between a high number of neurons. These neurons are formed and construct an organ (with other cell types) in the process of embryonic and fetal development. Neuron formation, placement and connection is influenced/guided by some genes. But that does not mean that "a couple of genes carry the information to construct a brain". Genes control the cell, not the organ. Genes affect the cell structure and cell's operation; cell structure and cell's operation affects the organ development; organ's structure affects its functions and products.
Some reading on organ development can be helpful to understand this point (for example; Forces shaping the Drosophila wing).
But, if you refer the genes which guide the brain development as genes that create consciousness, then yes, there are consciousness genes. But, of course, this won't solve anything.

When you look in the mirror, you see yourself. That puts you in the company of animals like dolphins, elephants, chimpanzees, and magpies, all of whom have shown the ability to recognize their own reflections.
The mirror test is often used as a way of measuring whether animals possess self-awareness. Some fish have recently passed the test, which has left scientists confused about limits of "self consciousness".
https://en.m.wikipedia.org/wiki/Mirror_test
Other animals have far less of it, and it correlates with logical thinking and intelligence too. It's like a side effect or component of animal intelect and wit.
DNA codes intelligence hardware and number of neurons, just like number of teeth and pilosity. On the next hyperlink theres info about 22 genes for intelligence and "dna for brain volume"
Intelligence is the key to human survival since 500+ billion years:
Making spears, fire, tools, clothes, and avoiding death from other monkey tricks.
DNA of brain size and logical ability has incrementally been sharply selected and increased for humans.
https://www.google.com/search?ei=xP68XZfAEcLggweFsqTwAQ&q=intelligence+dna
Theres even articles on logic gates within DNA. Self-concious often signifies introverted emotion, so it's rarely used in biology journals. Self-aware is used in animal psychology tests, and is relative / not an exact science.


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What does it mean to be a fully human monoclonal antibody?
I somewhat understand that some monoclonal antibodies are developed from the cells of mice, or a fusion of human and mice genes.
When something is a fully human monoclonal antibody does that mean it came from some person? What type of human cell did it come from? Will the drug always be from that original human?
I read that they're derived from something called a phage display technique. I'm guessing this is another type of way to fuse genes together, but with all human cells.
Where do the cells come from?

Following technquies are used for developing fully human monoclonal antibodies:

Complementarity-determining region (CDR) engraftment: This method is
performed by preparing  cDNA library. CDRs are amplified from a mouse
hybridoma cell line, and later these sequences are engineered  into
the human variable light and heavy chains.
Using transgenic mice with human Immunoglobulin genes:  Hybridoma fusion
technique is used to synthesize human monoclonal antibody. The
transgenic mice expresses DNA encoding human immunoglobulin genes.
Display technologies using phage, yeast, and ribosome:  Heavy and
light chain cDNA from human B-cells is used to construct a library.
Various  heavy and light chain pairs are expressed on the phage.
These phage are screened for antigen binding. Further this
recombinant monoclonal antibody is synthesized using prokaryotic,
yeast expression system, insect or mammalian cell expression system.

Display technique uses the  principle of specific antibody production but employ micro-organisms in case of phage display and cell free extracts in case of ribosome display. These systems depend on  creation of gene libraries  constructed using peripheral blood from humans. The  products synthesized in this procedure are antibody fragments of Antigen binding (Fab) or  Single-chain variable (scFvs), having complete human sequence.
Via:
http://www.pharmtech.com/novel-process-developing-fully-human-monoclonal-antibodies?id=&sk=&date=&pageID=3

Took a while to do some additional reading, but thank you. I think I better understand. Would you mind letting me know if you don't fully understand this though?

Also, Link seems dead.

I found this small article that seems to cover all your questions:
https://www.sciencedirect.com/topics/medicine-and-dentistry/human-monoclonal-antibody
Summary:
Being considered a human monoclonal (many of the identical antibody, as opposed to different antibodies for the same target) antibody does not mean it is produced by a human body; it means that the fc-region of the antibody is human-like, which aims at avoiding immune reactions against that antibody if injected into humans.
So the human antibody can originate from animals (e.g. rats or rabbits) with humanized antibody genes or from immortalized human cell-lines (lymphocytes).

Thank you. I was able to access the full article, and was surprised to see it's from 1998. It has some sections on general approaches to making monoclonal antibodies and human monoclonal antibodies. The 1998 article explains that for ethical reasons it's not possible to "hyperimmunize humans and typically the only source of B lymphocytes is peripherial blood ... less suitable for fusion." It then goes on to discuss workarounds. The only human work around is to "immortalize" the B lymphocytes with the Epstein-Barr virus.

The link you shared has newer information, and talks about using "bacteriophage display library of human variable region sequences and selects for antigen binding in vitro. The selected genes are then combined with human constant region genes to reconstitute a complete IgG antibody." This sounds like the current state of the art. Doesn't sound fully human either!

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Sorry, I didn't know that and obviously just tried to help.

@KaPy3141 That's fine - my comment is one of the standard ones and is intended to help you know so you can improve your answer, since you can edit it to fix the problems. Welcome to Biology.SE!


text:
Why did Darwin say "the misfortune to undertake"?
Why did Darwin say "the misfortune to undertake"?
"Every naturalist who has had the misfortune to undertake the description of a group of highly varying organisms, has encountered cases (I speak after experience) precisely like that of man; and if of a cautious disposition, he will end by uniting all the forms which graduate into each other, under a single species; for he will say to himself that he has no right to give names to objects which he cannot define."
One reason, is that he was challenged with a difficult task.
Another is that he is unhappy because he could not name more than one species and had to say they are all one species because they graduate into each other.

This would perhaps be better suited the the English Language and Usage site.  It's simply a literary device, a way of saying that he was faced with a difficult, frustrating task.

I'm voting to close this question as off-topic because it is a question of literature, not biology.

If you read the subsequent paragraph it is clear that he is speaking of the difficulty in drawing borders between species.
It is not possible to draw definitive species boundaries, especially if you follow species over time  rather than classifying organisms with a snapshot in time: these issues come up time and time again on this Stack. Some examples:
How could humans have interbred with Neanderthals if we're a different species?
Usage of "lineage" over "species"
Transitivity of Species Definitions
Because all species descend from common ancestors, there is a time at which any two organisms shared an ancestor. For related organisms, you can recognize that shared history, emphasize the similarity and at some point group two subspecies together as one species, or you can focus on differences and separate them. Whichever you choose, someone can argue that the species should instead be separated or grouped.
Ultimately, the distinctions are based on somewhat arbitrary decisions, and counterexamples are abundant whichever rule you try to use (for example, a rule that organisms that have viable offspring should be considered species renders many examples that one would argue should be separate species, and examples of individuals that should be one species that are nonetheless not able to produce viable offspring).
It's not so much the misfortune of the task being difficult but rather of it being not possible to come to a definitive answer.


text:
Bug identification: how to identify this bug?
I found this cast/shed skin from molting in my house:

The house is in the countryside by the beach in Portugal with a temperate and humid climate and mostly pine trees and eucalyptus. Humidity is 84% and temperature around 21ºC indoors. The size is 1-2 cm.
From bugguide.net it looks like a beetle. I also tried InsectIdentification.org but it's limited to US, Canada, and Mexico.
Can anyone identify the cast skin? And does such bug identification require an expert or can an amateur use some resources to do it?

It is not a cast skin, as adults do not molt, and this is an adult beetle. You can tell because it has elytra (forewings), and only adults have them. It reminds me of a Scarab.

I can't see the forewings, but I trust your judgment! Would you like to write an answer? And what resources would you recommend for a newbie to identify bugs?

Trying to identify this specimen much past family (and I agree with @Karl WRT that) might not be possible, as the head appears to be missing; in addition, this appears to be the remains of a spider's meal (there are obvious fibers -- probably silk -- visible in both photographs).


text:
How was it discovered that flouride helps stop tooth decay?
Apparently flourinated water helps stop tooth decay. So I have some quesions about this.
Firstly how does it stop tooth deacy?
and
Secondly, how was it found that out of all the chemicals, it is flouride that stops tooth decay and nothing else?

What research of your own have  you done on this topic? If you look at the related questions on the sidebar you will see that there is one entitled "How does fluoride prevent tooth decay?" which is your first question. Please check out previous questions before posting.

Possible duplicate of How does fluoride prevent tooth decay?

@David that's a totally different question.

Please don't post answers in comments. @zooby it seems like you have 2 questions here, one of which is answered already elsewhere. If your question is totally different, then that part you wrote in your body must not be part of your question, so you should edit it out. Otherwise, people might think it looks like the same question and it will be closed as a duplicate and you won't get an answer to your actual question.

There is an interesting historical story of fluoride use in prevention of dental caries.
Interestingly the journey started with a "mysterious disorder-fluorosis."

In 1909 Dr. McKay (r) persuaded the Colorado State Dental Association to invite Dr. Green Vardiman Black (l), one of the nation's most eminent dental researchers, to attend 1909 convention where McKay's findings were to be presented. The two men began joint research and discovered other areas of the country where brown staining of teeth occurred.

Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs, Colorado

McKay collected the samples. And, within months, he had the answer and denouement to his 30-year quest: high levels of water-borne fluoride indeed caused the discoloration of tooth enamel.

Dr Dean recalled from reading McKay's and Black's studies on fluorosis that mottled tooth enamel is unusually resistant to decay. Dean wondered whether adding fluoride to drinking water at physically and cosmetically safe levels would help fight tooth decay.

This finding, considering the thousands of participants in the study, amounted to a giant scientific breakthrough that promised to revolutionize dental care, making tooth decay for the first time in history a preventable disease for most people.

These are excerpts from the article
Another reference
In 1802, Sir James Chrichton Browne suggested the probable cause of dental caries as a change in bread, which did not have bran or husky part of wheat containing fluorine.
Now your next question on fluoride stopping the tooth decay.
So yes apart from preventing tooth decay, research has found that fluorides like silver diamine fluoride can be treatment of choice for dental caries.

The silver component provides an anti-bacterial effect while the fluoride promotes remineralization of tooth structure.

I hope I have answered your question :)

@zooby you may accept the answer if you are satisfied so that in future this will motivate others to answer your questions


text:
What organism is this?
This is something I found growing under my kitchen’s sink. It looks like a growing potato and it’s really hard (tried to pull it down using a hard cardboard but in vain). I think a knife may work but I want to know what this is and if I should be taking any precaution.

I’ve put up a video of it as well here:
https://photos.app.goo.gl/JLqJrxeqnboRn9bg8

That looks to me to be non-biological but rather the result of using an expanding foam filler product to fill in gaps, as might occur in the wallboard where a sink is mounted.  Here's an example of such a product:


text:
Alternative to Lotka Volterra
Would you guys know any kind of differential equations that would dictate population growth without relying on Lotka Volterra ? Thanks ^^

I'm voting to close this question as off-topic because equations for population growth are not biology.

I think this question could use some improvement and background to make sure it's clear what the goals are; right now it seems overly broad. However, I disagree strongly that discussing equations that are highly relevant to biology is not biology, unless that discussion is not directed at a biologically relevant problem.


text:
Why does music give you emotions?
Why do we feel emotions when we hear music?
Click to see video
How can a set of tones arranged in a specific order and timing make you feel sad or happy?
I read that music can somehow trigger the part of the brain which is responsible for language processing. Whatever be the mechanism of emotions, why do we feel that certain emotions are connected with certain tunes?
What may be the evolutionary origin of this?

I am voting to close this question as off topic. This doesn't concern biology on its own, it involves Neurology and Psychology. I am aware that the first one is still concerned by Biology as a whole, albeit I think it would be better to ask such question in a more specific environment, such as https://psychology.stackexchange.com/

The evolutionary origin is alleged to be recent: Other animals do not have a preference for dissonance and consonance.  (McDermott & Hauser, 2004).
Humans have new auditory regions in the brain for predicting and processing speech, and processing the emotions conveyed in the voice. The human voice mostly has harmonics in the 3rd and 4th note due to the properties of the vocal tract. There have been some basic studies of the 12 notes of the piano as represented in the human voice, which concluded that the "consonant" sounds from chords and melodies correspond to the the sound of the human voice.
This article suggests that dissonant/amusical frequencies are uncommon in natural ecology, because of the way physical objects resonate. Bird melodies are atonal and not particularly dissonant or consonant.
Some people may suggest that animal alarm calls are more dissonant than mating calls, especially those that are made to scare you like a cat hiss, a gecko scream, baby marmots which are separated from their mother, a rabbit being eaten.
Actually, many studies have identified brain regions used for emotional processing, the same that react when they see a beautiful or unnerving image, by MRI tomography and also from people who have had strokes which make them non-reactive to music, and people with amusia known as amusics.

They also
  found an increase in frontal-midline (Fm) theta power
  for consonant music, indicating greater coherence of
  neural firing in certain population of neurons. This is
  interpreted as reflecting activation in the anterior cingulate cortex (ACC), which has been implicated elsewhere in processing pleasant music (Blood & Zatorre
  2001). The ACC’s role in emotion is also supported by
  its inputs from other key emotion-related areas, such as
  the amygdala, hippocampus, and parahippocampal gyrus (Devinsky, Morrell, & Vogt, 1995).

There are a lot of studies on the topic, this is a well written summary of recent research.
Musical sensory stimulation is a fascinating topic with complex ecology and brain quirks, it's best to research the topic individually to find which aspects of music do what to the brain:
Music rhythms vs cardio/breathing/cerebral rhythms, individual sound consonance/dissonance, and complex auditive patterning of sounds found in rhythmic chords and melodies. The conflict-resolution of harmonies are what you are referring to regarding the sequence of notes, there are studies on musical expectation, it's a sub-field of consonance/dissonance neuroscience.


text:
What controls specific gene silencing during cell differentiation?
I am intrigued by the fact that all cells of our body use the same DNA. How do the cells differentiate during the post fertilisation divisions?
I read about gene silencing, which can be an answer to this. But still I do not understand how the cells decide which gene it is supposed to silence, by making the micro RNA.
Consider a zygote that is beginning to divide. I would assume that the chemical and physical context of each daughter cells would be more or less similar in beginning. Then how can there be a differentiation? Is there some supervising authority present in the zygote that decides what to make out of each daughter cell?

Possible duplicate of which exact mechanism triggers the first cell differentiation after n divisions?

The cells differentiation during post fertilization period is govern by a set of regulatory genes called Homeotic genes.These are genes that "select" the identity of entire segments or structures in the bodies of developing organisms.
These gene encodes a transcription factor that is expressed in a specific region of the organism starting in its early development i.e. embryo stage. The transcription factors change the expression of target genes to enact the genetic “program” that's right for each segment.

The homeotic transcription factors shown in the diagram above[homology between Hox genes in mice and humans] contain a DNA-binding protein region called the homeodomain, which is encoded by a segment of DNA, called the homeobox.The animal genes containing homeobox sequences are specifically referred to as Hox genes. This family of genes is responsible for determining the general body plan, such as the number of body segments of an animal, the number and placement of appendages, and animal head-tail directionality.
In addition to this genes, the early developmental cascade include the following genes:

Maternal effects genes:These are genes whose mRNAs are placed in the egg cell by the mother before fertilization. Some of the mRNAs are “tied” to the head or tail end of the embryo and are responsible for setting up the head-tail polarity. The maternal effects genes encode regulators of transcription or translation that control each other as well as other genes.
Gap genes: They are activated through interactions between the protein products of the maternal effects genes, and they also regulate each other. They're responsible for defining large, multi-segment regions in many organisms.
Pair-rule genes: These are turned on by interactions between gap genes, and their expression patterns are refined by interactions with one another. They appear in multiple “stripes” along the embryo, similar in pattern to the segments of the adult organism.When a pair-rule gene is missing due to mutation, there is a loss of structures in the segment regions where the gene is normally expressed.

For further information you can refer this link:
-  Click here 1
- Click here 2
-  Click here 3

Hox, pair-rule and gap genes are all expressed well after the first differentiations.

Activation and deactivation of different genes commands the process of cell differentiation. Gene expression responsible for cell differentiation is  controlled by intrinsic and extrinsic signals. This regulated signalling from inside and outside the cell is responsible for embryonic development.
Environment around the cell, such as small molecules, proteins, temperature and oxygen control the gene expression.  Cellular communication takes places to decide the fate of particular cell by interplay of signals between the proteins synthesized around the cell. These proteins can be morphogens, growth factors or cytokines. This extrinsic signalling sets off intercellular signalling that stimulates expression of genes. Alteration in gene expression by turning gene on or off, regulates the production of gene product.
Gene expression is regulated intrinsically by modifying DNA. DNA and chromatin are altered chemically. Change in chromatin effects gene expression by controlling the binding  of genes to transcription factors. These epigenetic  chemical modifications are known as DNA methylation and histone modification. Chromatin modification plays important role in gene expression during cell development.  For example, proteins responsible for chromatin modification  play important role in muscle cell differentiation. Transcription factors MyoD and MEF regulate enzymes responsible for chromatin modification, such as histone acetyltransferases and deacetylases.
Via:  https://www.nature.com/scitable/topicpage/gene-expression-regulates-cell-differentiation-931/#
Chromatin modification helps in continuous gene expression which is required during cell differentiation. The gene silencing involved in embryogenesis, promotes cell development into mature cell types. This silencing of gene is done by making gene inaccessible to transcription machinery, and when genes are needed again in adult cell type the chromatin modification opens DNA and make it available for transcription.
Embryonic cell types have particular regions for chromatin modification that regulate gene expression required for embryonic development. These regions can modify gene expression by activating or silencing genes.
Via: (https://www.ncbi.nlm.nih.gov/pubmed/16630819)


text:
Neisseria meningitidis transformation into a pathogen
I read the wikipedia article about Neisseria meningitidis, and it says that

N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 5–15% of adults

In some cases however, it infects the bloodstream, creating a Meningococcemia disease which is highly lethal. It may also create a meningococcal meningitis.
The article also says that this disease is somewhat infectious. Not as infectious as common cold, but it is known to cause epidemics in Africa and Asia.
My question is: How can it be so abundant in its non-pathogenic form (up to 15% of adults) yet cause epidemics? It seems that it's transmitted from nose to nose somehow and doesn't cause a disease, yet when it does cause a disease it also causes a disease upon transmission.
It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people. Because then it wouldn't cause epidemics, since the majority of the population is immune to it as evidenced by the fact that it's part of their microbiota.
Does N. meningitidis mutate to become pathogenic? Do the nasal strain and the pathogenic strain have different genotypes?
I tried searching for an answer but didn't find any.
Thank you very much.

Welcome to Biology.SE! This seems like an interesting question, but I would note that 5-15% is not "the majority of the population" ...  ——— You may benefit from taking the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

If you can come up with a well supported (referenced) answer to your question I encourage you to post it as an answer here. ——— The wikipedia article on epidemics may be of interest. You also might want to read up on epidemiology and opportunistic pathogens — many "infections" by disease causing organisms can be asymptomatic (e.g. typhoid).

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people.

Well, actually, it is kind of like that.
The answer is complicated, but can be boiled down to, virulent serotypes of Neisseria meningitidis infect susceptible populations. For the short answer, just read between the highlighted boxes.

Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival.

Virulent serotypes have capsules that help them evade detection and destruction; they have an outer envelope that helps them invade and infect susceptable individuals.

The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host.

The most susceptible populations are infants/babies (most frequently), young children and unvaccinated young adults (during outbreaks). These are the populations most likely to have no to low antibodies against the bacteria.

The meningococcus remains a common cause of bacterial meningitis in children and young adults in the USA (132), now mostly affecting children less than 2 years of age (102, 133). Two-thirds of meningococcal disease in the first year of life in the US occurs in infants less than 6 months of age (134). Worldwide, the rates of meningococcal disease are also highest for young children due to waning protective maternal antibody, but in epidemic outbreaks, older children and adolescents can have high rates of disease. Fifty percent of cases in infants in the US are due to serogroup B; serogroup C is mostly seen in adolescents and serogroups B and Y in older adults. Even though peak incidence occurs among infants and adolescents; one-third to one-half of sporadic cases are seen in adults older than 18 years.

Carrier state isn't lifelong or even year long, in fact, it can last as little as a few weeks.

When approximately 10% of individuals from the general population at any time were carrying N. meningitidis in the nasopharynx (Cartwright et al., 1987), the carriage rate was shown to be <3% in children younger than 4 years and increased to 24–37% in the age-group 15–24 years... Then carriage rates decrease to less than 10% in older age-groups.

and

Meningococcal carriage increases rapidly among university students in the first month of the academic year and much of this increase probably occurred during the first week (Neal et al., 2000). The study, performed at the University of Nottingham, UK, showed the carriage rate increased in the first week of term from 6.9 % on day 1, to 11.2 % on day 2, to 19.0 % on day 3 and to 23.1 % on day 4. High social mixing probably caused this increase.

Carrier state is influenced by protective antibodies, local mucosal factors, and lower virulence of the bacteria in carriers. Smokers, for example, are more likely to be carriers than non-smokers. The type of N. meningitidis  also influences carrier vs. infected individuals.

In Norway, approximately 9% of the carriage isolates belonged to two of the known hypervirulent clonal complexes...

That is, of 100 carriers, less than 10% carry a very virulent type. Non-virulence or low-virulence is the norm.
A non-virulent strain can become virulent to others by sharing of DNA.

Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species. The human nasopharynx may harbour diverse pathogenic bacteria, like N. meningitidis, H. influenzae, S. pneumoniae, as well as non-pathogenic bacteria, such as N. lactamica and the moraxellae.

Again, carriers ave protective antibodies.

Immunity to invasive meningococcal disease is dependent upon the presence of serum immunoglobulin G (IgG) which elicits bactericidal activity toward the infecting organism. Infants may be protected from meningococcal disease by the presence of maternal IgG which is obtained passively during gestation and lactation. Maternal immunity will be replaced by acquired immunity. Exposure to non-pathogenic Neisseria and other cross-reacting species in the nasopharynx increases the level of specific antibodies during childhood (Sanchez et al., 2001, 2002; Troncoso et al., 2000).

And

Carriage of commensal Neisseria, especially N. lactamica, is associated with a high titre of antibodies against N. meningitidis. Highly homologous structures are present in N. lactamica and N. meningitidis (Troncoso et al., 2000, 2001). Sera from mice immunized with N. lactamica and boosted with N. meningitidis have been shown to kill meningococci.
...Mucosal immunity is not able to prevent the colonization of the nasopharynx by meningococci, but it plays an important role in preventing the invasion of epithelial cell (Griffiss, 1995).

If that answers your question, that's what I hoped for, because the rest is a mystery  to me. But remember, you aren't a lifelong carrier. You might be a weekslong carrier, and every exposure to a non-virulent serotype increases your immunity.
Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis: an overview of the carriage state

Thank you for your answer. I'll have to reread it a few more times and also explore the sources your referenced before accepting though. Thank you very much for such a detailed answer.


text:
What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)
What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)

The insect in the picture was slightly damaged after an altercation with a human.

This is a cockroach.
Although about 30 species typically associate with humans and human habitats [source], the only ones that I know that have strong parallel dark lines running in the rostral/caudal direction are the Asian cockroach (Blattella asahinai) and the German cockroach (Blattella germanica).
According to Wikipedia, these 2 species appear very similar. At the adult level, it's actually more behavior (B. asahinai is a better flyer and tends to fly toward light) and habitat (B. asahinai prefers living outdoors while B. germanica prefers living indoors) that "best" differentiates these two species.
Your specimen is not an adult, however, as is made very clear by the extension of the dorsal parallel stripes extending beyond the pronotom, by the relatively small size of your specimen (<10 mm long), and by the absence of clearly-developed wings [see here for descriptions].
This wingless and long-striped specimen is an immature nymph. Although UFL indicates that late instar roaches of these two species can be identified by the presence of white spots on the dorsal abdomen of the Asian roach, your specimen appears to be an earlier instar and does not yet have this spotted pattern.
As in the adult stage, the early instars of B. asahinai and B. germanica also appear quite similar:

 German (left) and Asian (right) early instar nymphs. Photograph by Dina L. Richman (University of Florida); [source].
German nymphs are slightly smaller than Asian roach nymphs, but again they are quite hard to tell apart (often times being less distinct that the above picture).
I've been told that the most useful way for differentiating is simply by location: if found indoors it's more likely German and if found outdoors it's more likely Asian.
Regardless, if it was found inside, you need to act quickly to prevent an infestation...


text:
What advantage does lactose have as the main sugar in milk?
Most organisms have lactose as their main sugar in their milk.
What advantage does lactose give have over sucrose (Which is a common sugar in the plants, so it makes sense for it to be present in milk)
Is lactose synthesis easy? Or is the enzyme B-galactosidase easy to make?
Or is it more easily digestible, allowing mammalian infants to get energy faster?

Possible duplicate of What selective factors drove the evolution of lactose in lactation?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). Please start by having a look at the "Related" questions automatically associated with your question — in this case your question has a duplicate and thus should be deleted. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

It doesn't make sense to have sucrose in milk if mammals are unable to produce it.

As @anongoodnurse states elesewhere, the comparison with sucrose is arbitrary. The question is better stated in terms of lactose v. other disaccharides, but unfortunately has been asked before. I would mention that ideas like "synthesis being easy", "enzymes being easier to make" and "get energy faster" are biochemically naive. (And most organisms do not produce milk. Try "mammals".)

If you feel the existing question and answer do not answer your question please explain why or expect the question to be closed.

Yes it is thought to provide safer milk, less vulnerable to every bacteria that respires and multiplies on sucrose, and which lets the baby grow faster due to higher sugar content.
Milk has evolved from pouch mucus, antimicrobal secretions of the immune system, Lysozyme in mucus is a glycoside hydrolase which ruptures bacteria cell walls. So the origins of milk are very different than for plants.
Lactose is a larger molecule than sucrose, so it exerts less osmotic effect per unit mass, allowing more carbohydrate to be included in am isosmotic secretion such as milk.
for example:
marsupials have mostly longer oligosaccharides and their milk contains 11-14% sugar,
zebras and and horses with only lactose achieve 7%
humans and other primates achieve 8-9% using milk and polysaccharides.
Another advantage is that it's a molecule rarely produced in nature, and fewer bacteria have evolved the enzymes required to digest it, upgrading the lac-operon to produce galactose-permease, save for beneficial lactobacilli, e-coli, and other mostly mutualist species.
full text.
It is thought that milk evolved from secretory glands in the synapsid egg pouch which helped to protect parchment eggs, with moisture and antimicrobial secretions. In fact, lactose is thought to have come from mucus sugars, which are used to encapsulate and neutralize microbes in the body, "Because α-lactalbumin evolved from lysozyme before the division of amniotes into synapsids and sauropsids (see Figure Figure1),1), the capacity to produce lactose was an ancient trait that preceded its utility in milk synthesis"
Intro to synapsid and sauropsid precursors of lactose.

"and not many bacteria have evolved the enzymes required to digest it" There is clearly no problem for bacteria in evolving lactase/beta-galactosidase — the whole dairy industry depends on that — so this argument clearly does not hold. For the rest your answer does not explain why lactose is preferred to sucrose — the poster's primary concern. The complex argument proposed in the question that this is a duplicate of, implies that there is no obvious easy answer.

If you want to contradict what a professor of dairy chemistry states, the author of the stated arguements, it would be wise to have some fact to support your arguement. For the rest my answer explains that sucrose tends to osmotically travel through the membranes into teh cell walls and presumably to the capillaries, and lactose doesn't because it's too big thereby increasing the energy content of the milk, and also that botulin and every bacterial that respires and grows on petri dishes can process glucose and infect udders adn babies, but not lactose.

This answers a question, but not the OP's question. The OP is comparing mammals to grapefruit, then asking why.

The two factors convey a huge gargantuan advantage compared to a banana/fig. If common bacterial resistance is not an advantage, then what is it? A baby and udder without botulin issues sounds like a good idea to me. Ease of containment and transport of sugars due to lower osmotic pressure is also an advantage, because it allows for more energetic milk than with sucrose, and therefore allows the child to put on weight faster, and more safely.

The validity or not of arguments  depends on their logic, not on who makes them. The one at issue is rehearsed in an answer to an earlier version of the question. I have not commented on that answer, only on the defects in yours. In particular I criticized the original statement about the lack of bacteria that can metabolize lactose, which now seems to have morphed into an equally contentious argument about the bacteria with sucrase v. those with beta-galactosidase. To this I would query the statement that "lactose is a larger molecule". Lactose and sucrose have the same molecular weight.

The original version of your answer — to which my criticism was directed — contained no mention of the hypothesis of Urashima et al., quoted by Alan Boyd in his answer to a similar question. It did, and still does, contain the false assertion that “lactose is a larger molecule than sucrose” — an assertion Urashima et al. certainly did not make. In fact both lactose and sucrose have  molecular weights of 342.3! As you now seem to be leaning on the hypothesis of Urashima et al., would it not be better to vote to close this question as a duplicate, rather than rehashing Alan Boyd’s answer?

One of the advantages of lactose in breast milk is that it is digested slower than sucrose and its ingestion results in lower fluctuations of blood glucose levels thus being a stable source of energy.

Lactose, a disaccharide of glucose and galactose, is uniquely present
  in mammalian milk. Human milk provides the infant with about 40%
  energy as lactose and 50% from fat. With 6-7 g/dL lactose, the breast
  fed infant consumes high carbohydrate/kg body wgt, suggesting
  carbohydrate induced hepatic lipogenesis would be problematic with a
  high fat milk diet. However, galactose, unlike glucose is
  non-insulinogenic and shows high hepatic clearance. We propose
  lactose in human milk confers unique metabolic advantage to the infant
  by delivering non-insulinogenic carbohydrate which can be slowly
  metabolized in the liver to glucose or to support fatty acid
  oxidation. We determined insulin, glucose, triglyceride, free fatty
  acid and amino acid responses in 16 healthy adult men given in random
  order 650 mL carbohydrate-free infant formula reconstituted to contain
  50g lactose, glucose, sucrose or corn syrup solids. The milk formula
  was given 3 hr after a lactose and sucrose-free meal, then again after
  3 hr, to model the carbohydrate load and continuous feeding of
  breast-fed infants. Blood was drawn every 15 min, and total and
  incremental area-under-curve change in insulin and glucose determined.
  Lactose gave a significantly lower rise in plasma insulin and glucose, in the first and particularly second 3 hr following intake,
  compared to glucose or corn syrup solids (P <0.001). Individual
  variability in triglyceride responses was high, with no difference due
  to carbohydrate in this 6 hr study. We show lactose enables
  maintenance of glucose and insulin equilibrium, avoiding high
  postprandial peaks achieved with glucose or corn syrups in milk fed
  at 3 hr intervals. We propose an important metabolic homeostatic role
  for lactose as carbohydrate source in human milk.

The lower glycemic index of lactose (46) compared to sucrose (65) also reflects slower conversion of lactose to blood glucose (gisymbol.com)


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Lab technique to distinguish between single stranded and double stranded DNA?
What lab techniques exist to differentiate between single-strand and double-stranded DNA?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). For instance searching with "differentiate between single-strand and double-stranded DNA" led me to this. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

Single and double stranded DNA have different electrophoretic mobilities, ssDNA will move faster on an agarose gel, so if you know the length of your DNA and it moves further than you expect
 relative to a dsDNA ladder it's probably ssDNA. The hyperchromic effect means that ssDNA also absorbs more strongly than dsDNA, so you can heat up your DNA and if the absorbance changes it was dsDNA and if it doesnt then its ssDNA (you should take an aliquot for this so that you have the rest of your sample in tact). You could also take an aliquot and add a single stranded exonuclease and run the products on a gel together with the DNA before the digestion, if nothing is present after in the digested well then you had ssDNA if there is still a band after then you had dsDNA (i don't think this method is really used as you could just run it on a gel which is simpler and you lose less sample, but it should still work).

+1 but I'd like to add an important caveat:  intercalating dyes that allow visualization of dsDNA on a gel may not bind strongly or at all to ssDNA.  So if OP does plan on doing gel visualization of mixed single- and double-stranded nucleic acids, consider using a dye like ethidium homodimer-1 or -2. Good source for dye selection here.

yes thats true you do definitely see a weaker band, so you do have to load more DNA or use a more sensitive dye. I've done with a couple of 100 ng with sybr safe and that has been fine, but it depends if you have that to spare.

@Dirigible Actually the fact that certain dyes bind ssDNA & dsDNA with different strenght can itself be used to differentiate between them. (As long as concentrations are known / comparable). Many qPCR systems also rely on that to measure melting curves, i.e. using dyes like SYBR

@pepsiandsoda I have a doubt...Wouldn't the absorbance also change for ssDNA as we heat it because it is also in some weird coiled shape and that shape must be due to hydrogen bonds which might not let the ssDNA to absorb the light fully. With increase in temperature, these bonds will break and absorbance must increase, although the increase might be small...


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What are cells not affected by hormones called?
Cells that are affected by hormones are called target cells which have their own receptors that listen to signals. I'm unsure of the actual name of cells that are not affected by hormones, I tried searching around on pages relating to target cells and the endocrine system, but no one seems to actually give a name to these cells that don't have receptors.

How about non-target cells? I found several examples of that usage including:

A book section titled: 9.3 How are steroid hormone target cells differentiated from non-target cells?1
Containing the following line:

Thus, estrogen will stimulate mRNA and protein synthesis in a target cell, but not in a non-target cell.

A book chapter titled: Target or non-target: Hormonal signal perception and response in the determination of cell performance2

References
1: Brown, R., Brown, R. E., & Brown, R. E. (1994). An introduction to neuroendocrinology. Cambridge University Press., p. 149.
2: Osborne, D. J., & Thompson, D. S. (1992). Target or non-target: hormonal signal perception and response in the determination of cell performance. In Progress in Plant Growth Regulation (pp. 237-247). Springer, Dordrecht.


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What type of ants are these?
I live in NYC and these fellas started popping out near my computer screen and desk. They don't seem interested in food as my sister usually leaves candy wrappers around. They however are stinky, I tried to catch one with a tape and I can smell the odors they give off like 4 inches away. They got these stingers on their butt so I think they could be a species of fire ant. They're also really tiny. As shown on a q tip here.

(click to enlarge)
Finally could these be bites? They are really itchy and I get them overnight.

They look like termite, rather than ants.

@JackRod all wrong for a termite.

A close up on one of the ones that is curled up and dead would be a big help. a side shot would be best.

Many, ant species have stinger.

odorous house ant
Without a better picture I can't be certain but based on what anatomy we can see and you mentioning smell I would guess the odorous house ant.
They do stink when crushed, it should smell like blue cheese and turpentine.  They are common house pest in NYC drawn by sweets and water.
They do not sting or bite so they are likely non connected but again without a better picture it is hard to be certain. I suggest asking about medical concerns on the medical stack as they are off topic here.
As a small consolation at least they are a native ant species.

They should be Red Imported Fireants.
https://en.wikipedia.org/wiki/Red_imported_fire_ant

thorax shape is all wrong and head is too small for red imported fire ants. red imported fire ants should have pretty prominent petiole


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What is this white fluff growing in my basement?
I live in the countryside of Western Europe by the beach with a temperate climate. After a period of unusual humidity at 84%, I noted this white fluff in the basement floor:

The first picture is about 40 cm and the second 10 cm.
The basement is usually closed and keeps humidity. Temperatures average 18-20ºC, and humidity is now 77%. I assume it's a fungus since the floor was clear before and it seems to collapse when I rub my foot on it.
What is this species, and how can I prevent it?
Update: Following @anongoodnurse's suggestions, it's definitely a salt. I scraped the stuff, poured water, and it shriveled instantly. Here are photos before and after:

Here is a close-up of another piece, where the shards look like a crystal:

It did not smell indeed, and I did not taste it. I opened the basement door to ventilate the area, and I understand that it would accelerate the evaporation of the salty water.
I don't know if this growth has happened before, e.g. because of a leak in a pipe, or is a one-off occurrence, e.g. because of the unusual humidity in the last few weeks. I will check if the basement has any pipes.

What is that floor made of?  Looks like square vinyl tiles.  Has it been raining a lot during this period of high humidity?

The crystalline appearance makes me suspect that that is a mineral efflorescence rather than a biological growth.
See for example: https://www.ceramictilefoundation.org/blog/understanding-efflorescence-ugly-white-powder-on-tile

The floor is either ceramic or stone tiles, not vinyl.

@tyersome Efflorescence is intriguing. How would I test if it's a salt, by putting water on it?

@miguelmorin - Yes. Scrape a bit up (it should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water, it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in. If it dissolves and you're brave, you can taste a tiny bit then spit  and rinse. Fun!

Salt water is probably entering the basement through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates. If it turns out to be salt, you might ask over on DIY what to do about it. If you have metal pipes under the floor, it can't be good.

@tyersome - Oof, apologies! I just realized your link and mine were identical (an honest mistake.) If you leave an answer, I'll give you all my rep earned plus 10 (my upvote). You basically answered the question with two lines. The rest (of my answer) was fluff.

@anongoodnurse — No problem — I thought this might not be an appropriate question for SE.Biology, so I didn't bother to post as an answer. Your answer is much more complete anyway so I think you earned the reputation, but thank you for the offer!

@tyersome - I know you'll earn it shortly (I've read some of your answers), but it will put you over the rep needed to do magic at 2000K. ;-)

Might as well make this an answer.

...it seems to collapse when I rub my foot on it.

As @tyersome stated, it appears to be salt, not mold. Salt crystals would definitely collapse easily underfoot, and should be mostly quite dry, whereas mold would be... maybe squishy (?) but likely unpleasant in some way. Mold also smells, which you haven't mentioned, whereas salt is odorless.
To test, scrape a bit up (salt crystals should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water; it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in.
If it dissolves and you're brave, you can taste a tiny bit then spit and rinse. While salt isn't toxic, I can't vouch for what was in the grout.
My guess is that there may be a low spot or two in your basement where salt water is entering through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates.
If you have a magnifying glass, you should see crystals in the undisturbed deposit. If instead it looks soft and hairy, it is mold. I can't think of a white mold off the top of my head (well, Candida albicans, but that smells yeasty and is definitely not crumbly). Mold/yeast needs a substrate (food) to grow on, and wet grout isn't very nutritious. Mildew, sure, but mot big fluffy mold.
 I don't like this reference because it's not scientific, but it explains efflorescence well.)


text:
Is the plant-human relationship a form of parasitism or commensalism?
We all know that mankind gets a lot of useful products for satisfying its needs from plants. They can be in the form of timber, fruits, oils, resins whatever. The plants don't seem to be benefitted from these actions in anyways rather in some cases, they might instead get hurt(as for wood and timber). Some tribes even live on trees to stay clear from predators.
So, is this relationship a form of parasitism or commensalism?

This appears to meet this sites criteria for a [homework] question — as such you must demonstrate that you have made a significant effort towards answering the question.  In addition, there are ecological relationships that don't fall into a subcategory of symbiosis ... ———— You might find the material on a site like Khan Academy worth reviewing.

No, this isn't a homework question. I was reading articles on various ecological relationships and this thought crossed my mind.

Questions don't have to be homework assigned for a class to be considered homework on this site — please consult the help pages on [Ask] questions effectively on this site, I suggest starting with the page about homework.

It's a complex study because there are different relationships: wild harvests (mahogany), forestry harvests(douglas fir), agriculture harvests(apples), garden plants (poppies), invasive species.
https://www.agclassroom.org/ok/lessons/upper/symbiosis.pdf
example of how to dial in GOOGLE searches properly to research narrow topics.. time taken? 2 searches, 35 seconds. "commensalism paratism mutualism in forestry human agriculture"

will answer the same next time.


text:
Has human intelligence evolved as a costly male signal?
In this video at 42:06, Daniel Dennett posits that our big brains are:

The human artifice or version of the peacock's tail.

Peacocks have sexual dimorphism - it's males who exhibit the costly signal of showing off a big, colourful tail.
Now, humans are more special, because there are certainly no differences in the cognitive potential of men and women. Yet, there seems to be evidence for each gender being driven by different interests.
Thus my question: has human intelligence evolved as a costly male signal which has, over time, been passed to females?

You cite an opinion piece as "plenty of evidence"?

If you deem Scott's essay as an opinion, you haven't read it at all. Then, it's not just him - many other folks like Gad Saad have studied the topic in-depth and the conclusion is the same. On average, men and women have the same cognitive ability, but their interests diverge.

(Of course, I found it needless to say that there are exceptions and women's contributions to science are enormous - but little compared to men's)

Actually, I read most of the article. Though it cites research, it is an opinion piece. Opinion pieces cherry pick and misrepresent in order to support their bias. To truly evaluate the worth of this opinion piece, one would need to read all the cited studies (to see if there was misrepresentation, to see if it was a good study, etc.) As to your (horribly biased) statement that the fact that women have contributed less to science than men, you need to look no further than how women in science have been discouraged and discriminated against by men.

I don't engage in gender politics, so I'll stop here. I asked the question out of genuine curiosity. If the answer is "no", I'd love to hear an argument/ thesis for that. Similarly for "yes" or "we have no idea".

For example, read The Double Helix to see first hand how Watson stole - that is, used without her permission or knowledge - the work of Rosalind Franklin to deduce - to deduce the fact that DNA was a double helix. They could not have done it without her Xray crystallography work. As a Molecular Biologist and physician, perhaps I know a bit more about "gender politics" in Science than you.

In this study (well designed, well conducted), the author of the study himself misunderstood or misrepresented what the study actually revealed about brain differences between sexes. I had to read it several times to understand why it was so widely reported to demonstrate a significant difference in white vs gray matter in male vs. female brains, when it does nothing of the sort. The (male) author himself didn't understand?represent? the proper conclusion, and it's been cited as evidence almost 1000 times.

"I don't engage in gender politics..." You already did by claiming that the differences in scientific contribution between men and women is vast, or as you've said, "little compared to men."

There might be an interesting question buried in here somewhere (along the lines of "is intelligence a sexually selected trait in humans?") but it's buried in unnecessary non sequitur and unsupported claims about male and female humans.

@BryanKrause I sincerely apologise if it sounded like that. I understand it's a sensible topic. Happy to get an edit from someone with more expertise in the field, or for this question to get closed and reposted with a more proper description.

Female do use their intelligence to attract mates. Psychological studies have found that female intelligence is positively correlated with attractiveness for men

No
Think of it this way, what would you actually expect to see if this hypothesis was true?

Do humans actually show significant differences in relative brain size between sexes, like horn development in ungulates or tail feather length in peacocks, either currently or in the fossil record (answer: no).
Is intelligence a significantly sexually selected trait in other apes (answer: no).
Is intelligence a primary factor in mate selection (answer: not really. There is a positive correlation between intelligence and mate selection, but there are many other factors such as perceived social status, dominant behavior, personality, etc. that explain more of the variance. It's likely intelligence is more correlated with general health than a signal for sexual selection. This is why rock stars and athletes have large numbers of mating opportunities and scientists do not).
Are there significant selective differences between intelligence in males and females (answer: no. Intelligence is also positively correlated with mate desirability in male mate choice).

What these authors are arguing is that human brain size originally evolved as a sexually selected adaptation, and then selection proceeded so fast that it obliterated all evidence of it originally being sexually selected. Some authors I've seen argue this base argument on incredulity on the fact that human brain size evolved so fast. That's not a solid hypothesis based on evidence, that's just handwaving and argument from incredulity. It's making an argument based on special pleading to ignore the hypothesis with the simplest number of steps in favor of one that requires a more unlikely sequence of events to occur, and one that is not based on any actual evidence.
The idea that key features of "humannness" originally evolved in one sex and became established due to drag-along selection has been thrown around for decades with very little actual evidence. Richard Dawkins in The Ancestor's Tale suggested that bipedalism in humans originally evolved in males as a display behavior to look more attractive to females, and Owen Lovejoy has been promoting the hypothesis that bipedalism in humans evolved to allow humans to carry helpless infants. All of these cases are based on handwaving and little actual evidence.
Adding to this is the fact that in nature we generally don’t see “drag-along” selection, where selection favors a feature in one sex and it gets fixed in the other sex due to selection in the first sex. We especially don’t see it in traits that result in a huge penalty in reproductive fitness and hence have high selection pressure or represent a high-risk, high-reward adaptation. Nipples in male mammals may be one example, but nipples don't consume 20% of human's metabolic budget and put huge pressures on the female reproductive system.

Thanks for putting the time to write this thorough answer.

"has human intelligence evolved as a costly male signal which has, over time, been passed to females too, but whom are just not as interested to use it to attract mates?"
(I am ignoring that last part)
So you suggest intelligence (the modern human brain) evolved solely as a sexual dimorohism which then migigated over time?
I find that particular combination unlikely because intelligence would somehow need a sex-chromosome dependence which later was somehow lost. I don't think sexual dimorohism in intelligence can by seen in any mammals, and losing it again is unlikely as well.
But I can't disprove your idea completely: It seems the brain specific expression pattern is quite different in males and females. Also some brain specific genes were found as additional copies on sex chromosomes.
https://www.nature.com/articles/ncomms3771
With either of these 2 facts alone there is at least some miniscule potential that your hypothesis could be true!
(So you can argue gene duplication to autosomal chromosomes or expression levels being influenced by sex chromosomes.)
Ps: But it's equally (un-)probable that intelligence at first evolved in women only.

I don't know if this matters, but it bothers me: the N's all had neuropathology (autism, I'll assume Parkinson's, etc.) There are neuropatologies more common in men than women and vs. versa. Does this affect the validity of the study? I don't know, but I'd rather see this comparison done on normal tissue.  However, I don't doubt there are differences; testosterone has a significant effect on behavior which would imply the mind/brain. The study linked in comments shows a difference in white/gray matter use during certain tasks in men and women, but not a difference in matter per se.


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DNA of Different Species and The Fossil Record of Their Common Ancestor
Let me please be clear about something. I believe in evolution. The evidence and data are compelling and conclusive which makes it a very well-established theory.
I'm seeking a certain evidence (if it's existent) for evolution.
Assume we have two species (species A and species B) and we have full information of their genomes. I believe, by using their genomes, we can deduce when their most recent common ancestor lived (let's say X years ago).
Are their any instances in which this X number (which was produced mathematically) matched the age of some fossil (say species C) which has similar attributes to species A and species B? Any data about the ancient DNA of species C which may reinforce the evidence? Do we have something for humans and chimps?
I'm seeking a gourp of, arguably, unrelated quantitative data that point remarkably and decisively to common ancestor/evolution.
Thanks.

Possible duplicate of What could explain discrepancies between dates provided by the fossil record vs. the molecular clock?

One difficulty is that, even if a reliable molecular clock existed to predict when two species diverged, and if a fossil were found that seemed to match the phenotypic profile of a common ancestor, it would not be possible to conclude with certainty that it really is the common ancestor unless the fossil also provided DNA that could be compared to that of the two modern species.  It might be possible to find more modern examples though, for example by comparing the DNA of mummified Egyptian cats to that of modern cats.