text:
Are cytotoxic (killer) T-cells always present or are they only produced during a cell mediated immune response?
The book I'm studying says the following
"During a cell mediated immune response, the release of IL-2 by helper T-cells is resposible for stimulating the production of Cytotoxic T-cells, which have receptors that match the anti-gen of the infecting pathogen."
I'm not exactly sure if this is impliying that cytotoxic T-cells are only produced and present during an immune response or not, since I also have an older version of the book that simply says "the IL-2 released by helper T-cells activates cytotoxic T-cells" which seems to indicate that they are normally always present, but just inactive

Naive T cells are regularly matured in the thymus where they're released into the blood. A majority are CD4+, but many are also CD8+. As a caveat, many are TCRαß+, and few are TCRyδ+ (outside the scope here but fun to look up and read).  From there, they home to the lymph node where they hang in the T cell zone until blood trafficking signals coax them into the blood. T cells regularly navigate the body in response to signals from different cells such as blood vessel endothelium, lymphaptic vessel endothelium, epithelial cells, and so forth (1).
The basic process behind an adaptive immune response is that antigen-presenting cells get ahold of foreign antigens and head back to the lymphoid organs like lymph nodes. By the time they get there, they've matured into "licensed" professional antigen-presenting cells. They interact with both CD4+ or helper T cells, and CD8+ or cytotoxic T cells. It's more complex than that, but the point of the helper T cell is to produce "help" signals. These include IL-2, and other cytokines which not only assist the CD8+ T cells in their activation, but also determine a lineage they'll take based on other factors.
So they're both there, in the lymph node at the time the antigen-presenting cell, such as a dendritic cell, arrives to activate the lymphocytes in that region. Take home point: the naive lymphocytes are there until they are activated, in which you would be correct in your last line. But they do actually do things other than sit there, other take home point. They aren't simply anergic and waiting.

By other things, do you mean seeking and killing cancer cells and foriegn tissues and parasites (though these two I think could be the same thing as just an immune response, since they're foriegn) ? That's also breifly mentioned but just that, it isn't talked about much.

Well to be certain, cancer cells are subject to immunoediting, which is another complex term you can look into. There are also things handled by innate immunity and B cells. The naive T cells, however, can extravasate into tissues secreting chemokines in response to say, a pathogen. There are intra-epithelial lymphocytes and dendritic cells and macrophages that hang out in tissues like the gut mucosa and have the potential to active lymphocytes in situ. So "other things" can mean a great deal of things.


text:
Finding different Proteins with same function
Could you help me about finding two different proteins that coming from different ancestors, perform same function?
Thank you

There will be a lot!  Chromosomal dihydrofolate reductase and type II (plasmid) dihydrofolate reductase have not been derived from common  ancestor but catalyze completely the same reaction including stereochemistry by the authority of Brito.
Bacterial phenylalanine hydroxylase too is completely different in sequence of amino acids from phenylalanine hydroxylase from mammals (where plants have no such protin). The literature shows this paper Cloning and nucleotide sequencing of phenylalanine dehydrogenase gene of Bacillus sphaericus.

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text:
What is the purpose of Prostaglandin F2-alpha and the Prostaglandin F receptor in the melatonin cell signaling pathway?
I've been doing a lot of research recently on the melatonin cell signaling pathway for an extra credit project at school. I've included an image in this post, which is a diagram of the MT1 pathway. It seems to be a fairly standard GPCR sequence. I can identify all of the elements depicted in the diagram, but unfortunately I don't understand why some of these elements are present at all.
The portion of this pathway that stands out to me the most is the presence of a Prostaglandin F receptor (FP) as well as the presence of Prostaglandin F2-alpha (PGF2α). From the research that I have done, I've gathered that PGF2α is a prostaglandin found naturally in the body that can been used as an abortifacient in medical applications. I have not found any research that covers exactly why these two elements are present in the MT1 pathway.
Here's what I know: the Gi beta-gamma complex (Gβγi) and the Gq alpha subunit (Gαq) both activate Phospholipase C (PLC), which in this reaction causes the hydrolysis of PIP2 to create IP3 and DAG. My current hypothesis is that FP carries PGF2α into the cell, and PGF2α helps to activate PLC in some way. Unfortunately, I haven't been able to find any information online supporting this. Has anybody done any research regarding this topic, and if so can you provide any insight? I really, really appreciate it.

I don't have an expertise on this topic but check out the google scholar search. The top hit is this article: Melatonin blocks in vitro generation of prostaglandin by the uterus and hypothalamus. Apparently (from the google scholar hits), this relationship has been observed in vivo too.

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text:
Is the inhalation of ammonia a possible health problem for bats in an artificial small volume winter roost?
About 70 bats (Nyctalus noctula) spend their winter in an artificial small volume (0,050 cubic meters) winter roost located in the attic of a building. There is a single small exit to the outside directly from the roost. The roost has been cleaned before winter from bat droppings.
Is inhalated ammonia from bat droppings a potential health risk for them?


text:
What is this whitish jelly-like substance on a branch?

I came across this whitish jelly-like substance hanging on a fallen branch. I assume it was growing there and I feel like it might be a fungus or algae of some sort, or maybe an egg sack. I was hiking in a mountain rainforest in Hawaii. The area I found it was shady with adequate indirect sunlight, about 65-70°F at the time. There weren't any others nearby and it was the only one like it that I happened upon during the hike. What is this and if it is living, how does it grow, how does it live?

It is obvious, by the values, that the temperatures you give are not in Celsius degrees, but it would be nonetheless better to add the units.

Looks like a Tremella fuciformis, which is actually a sort of yeast that produces jelly-like fruiting bodies. AKA the white jelly mushroom.

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text:
Why was Achromobacter xerosis removed from the NCBI taxonomy?
The Global Catalogue of Microorganisms lists a bacterium called Achromobacter xerosis which is mentioned in several papers and patents. It once existed in the NCBI taxonomy database, with ID 216898. However, it is no longer there - going to https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 just yields a "No result found" page.
Why was this species removed from the NCBI's taxonomy? I haven't managed to find any documentation on why the NCBI would purge a species from their database, nor can I see any obvious reason to do so.

For whatever it's worth, I queried NCBI support about this and got a reply:

To: info@ncbi.nlm.nih.gov
  Subject: Reason for removal of a species from the taxonomy?
Hi,
I notice that the species Achromobacter xerosis used to be listed in the NCBI taxonomy at https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 but no longer is. I haven't been able to track down any documentation hinting at why a species would ever be removed from the taxonomy. Is there any such documentation that I've missed, and are you able to explain why this species in particular was removed?
Thanks in advance for your time,
  Mark

Reply:

Dear Mark Amery:
  The NCBI Taxonomy database records exist to support data that are in other NCBI databases. A review of the Taxonomy database must have identified that we have no records for which Achromobacter xerosis
  is designated as the organism name.
regards,
  Bonnie L. Maidak, Ph.D.
  NCBI Help Desk
  DHHS/NIH/NLM/NCBI

Achromobacter xerosis was proposed in 1954 by Groupé et al. Currently, the genus Achromobacter (revived by Yabuuchi & Yano, 1981) comprises 21 species, but A. xerosis is not among them. It seems that A. xerosis has never been validly published.

You've linked to your own website as a source for the claim that Achromobacter consists of 21 species, but I have no idea where I'm supposed to find that information. All I see is a download link for a password-protected PDF that I can't read since I don't have the password.

It's also unclear to me whether the lack of a valid publication is grounds for exclusion of a species from the NCBI taxonomy. As I interpret https://support.ncbi.nlm.nih.gov/link/portal/28045/28049/Article/1474/How-are-organisms-in-the-NCBI-Taxonomy-database-formally-named, it seems to suggest that valid names are preferred but that species without valid names may nonetheless be included in the taxonomy. As further evidence of this, note that https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi lists hundreds of species, not just 21! So I don't think that this is the full story.

@MarkAmery: If you hover with your mouse over the picture you will see this text: "Download PDF | Password 1". Alternatively, visit DSMZ: https://www.dsmz.de/

@MarkAmery: It is impossible for a validly published bacterial species not be included, intentionally or inadvertently, in the list of recognized bacterial species for a period of 64 years. Note that a proposal of A. xerosis name is not necessarily a valid publication of the new bacterial species. Search IJSEM for validation lists: if you find A. xerosis, it was validly published; if you don't find it, it was not validly published: http://ijs.microbiologyresearch.org/content/journal/ijsem

@MarkAmery: NCBI is not an authority in the field of bacterial taxonomy and nomenclature.

I'm not sure if you're missing my point or if I'm missing yours. Mine is this: NCBI does not seem to restrict itself to including only validly published species in its taxonomy, so as far as I can tell, whether A. xerosis was validly published is irrelevant to the question of why it was removed from the NCBI taxonomy. I don't see how your last two comments address that.

@MarkAmery: Each bacterial species comprises one or more strains, of which one is designated the type strain of the species. The type strain must be available in at least three recognized bacterial culture collections. If it is not available anywhere, and that can happen, the species is non-existent in the absolute sense: and that which is non-existent cannot be validated or invalidated; this could be the case of A. xerosis.


text:
Is their goli in plant cell?
We know that plant cells have dictyosomes instead of golgi but in my book it was written that plant cells have golgi apparatus?

Please try doing these before posting a question:

Consider the fact that this is not really a chatroom and posts should be written using proper and clear sentences (we can help if your English is not great but please put in some effort).

There should be some research effort from the side of the asker (did you try looking up reliable sources?).

There should be some context and explanation (for e.g. "We know that..." and "my book says"; I am not sure which "we" are you referring to and which book you are reading)

I am reading my course book

From wikipedia > Golgi apparatus

The Golgi apparatus, also known as the Golgi complex, Golgi body, or simply the Golgi, is an organelle found in most eukaryotic cells.

and further

In plants, Golgi stacks are not concentrated at the centrosomal region and do not form Golgi ribbons. Organization of the plant Golgi depends on actin cables and not microtubules. The common feature among Golgi is that they are adjacent to endoplasmic reticulum (ER) exit sites.

and also

The [trans Golgi network] may act as an early endosome in yeast and plants.

The dictyosome is a part of the Golgi apparatus. There is no english wikipedia for dictyosome but here is the french one


text:
What does +60mm mean in MRI scans?
What do the -30 to +60mm markings mean in this MRI scan image?

Short Answer
They are marking distance from a reference plane.
Longer Answer
In the images you provided, you are looking at horizontal slices through a brain. The legends are indicating that each plane has that vertical distance from a reference point (if the subject were standing); the positive numbers are dorsal to that reference and the negative numbers are ventral.
A common reference point for MRI images (to define as [0,0,0]) is the midpoint of a line through the pre-auricular point, though ultimately it is an arbitrary distinction.
If the actual reference point is important to you, you will need to verify the reference coordinate system used in the study you are looking at. It's also possible you are looking at coordinates transformed to some reference brain rather than real-life coordinates for that particular subject, but again, whether that matters or not depends on why you care. If you are doing research across subjects, you probably want to know reference coordinates; if you are doing brain surgery on a particular patient you want real-life coordinates.


text:
Was lactose present in the environment before the evolution of mammals?
Are there lactose sources other than dairy products in nature? I tried to search for it but I did not find anything. The question arose because I was wondering whether lactose-utilising enzymes in bacteria evolved only after the appearance of mammals.

Some seem to argue that lactose can be found in some vegetables and fruits too. A common reference to the sources I could find is a paper by Toba et al. (1991) titled Is lactose really present in plants? Unfortunately, the paper is behind a paywall for me so I can't tell whether the answer they give to this question is "Yes" or "No"!

According to Toba et al. per @Remi.b the answer is no.  Reinvestigation of reports of lactose in a few species came up negative.

@BryanHanson Thanks. Do you want to make it an answer or should I (you are probably more able to write an answer as you have access to the article)?

@Remi.b I'll put it as an answer with nod to you.

Is your question as in your title "is there non-milk lactose in Nature?", or is it "did the lactase gene exist in bacteria before mammals appeared?"  As you explain in your reasoning. The two are not necessarily the same.

The main question is the former, however, I cannot see how would it be plausible that lactase gene evolved before it had a substrate available on which it could work, and so before the organism bearing it had a selective advantage over its competitors. Clearly the reverse is not true, so it is possible that lactose was present but there wasn't a bacterium that evolved lactase before mammal uprising.

I think your logic is unsound. The question of the existence of lactose elsewhere in Nature I find relatively uninteresting. What I do find interesting is that enzymes that can hydrolyse lactose are found even in thermophiles (and indeed are being exploited for industrial dairy use). What they are doing in such bacteria is the question I address in my answer.

Preamble
This is an answer to the motivation expressed in the question:

“…whether lactose-utilising enzymes in bacteria evolved only after the appearance of mammals”

rather than that in the title. The presence or absence of lactose elsewhere in Nature will not decide this question.
Answer
The name lactase is applied to the mammalian enzyme that is able to catalyse the hydrolysis of the disaccharide, lactose, to glucose and galactose, allowing the digestion of this milk sugar by the suckling infant. However bacterial and plant enzymes that are normally referred to as β-galactosidases can also catalyse the same reaction.
The role of the β-galactosidases in bacteria such as Lactobacillus lactis that are found in a dairy environment may well be to hydrolyse milk lactose, as may be that of Escherichia coli, found in the human gut. However this is unlikely to be generally true for all bacteria. This is because β-galactosidases are found in a wide spectrum of bacteria, including extremophiles† which cannot possibly have had access to milk lactose.
β-galactosidases are generally members of a group of enzymes termed glycoside hydrolases and have been categorized into a number of families on the basis of sequence similarity. The enzymes in these families differ in their substrate specificity. To explain the existence of such enzymes in bacteria which do not have access to lactase it has been suggested that their natural substrates may be other disaccharides. This is actually the subject of a PhD Thesis by S.A. Shipkowski, who suggests that some β-galactosidases may actually hydrolyse β-1,4 galactobiose:

The significance of this is that the polysaccharide, pectin, found in certain plant cell walls, could be broken down by by other enzymes in the bacteria, yielding galactobiose.
Conclusion
Although the β-galactosidase in certain bacteria may be optimized to hydrolyse milk lactose, the gene encoding it is almost certainly derived from an ancestral glycoside hydrolases gene, the product of which predated the appearance of mammals and was used to hydrolyse other disaccharides derived from polysaccharides originating from various sources.
† It should be emphasized that the β-galactosidase from extreme thermophiles such as Thermus thermophilus KNOUC114 — isolated from a hot spring — hydrolyses lactose well. Indeed, its thermostablity has attracted interest in its development for use in the food industry (Ahn et al. 2012).

The Shipkowski PhD thesis that you linked, it says on the tile page that it was written to fulfill "requirements for the degree of doctor of philosophy"...? What is the relevance of the thesis to philosophy, though?

@ning — Natural philosophy provides the ‘Ph’ in PhD or the ‘Phil’ in D.Phil. I would also quote Shakespear here “There are more things in heaven and earth… than are dreamt of in your philosophy.”.

Here is the abstract from the article that @Remi.b found:

The presence of lactose in Forsythia, Achras zapota and Zizyphus
  jujuba has been reported previously.  We have reexamined its presence
  using gas-liquid chromatography, paper chromatography and high
  performance liquid chromatography.  Although all three plants
  contained glucose, fructose, myo-inositol (except A. zapota) and
  sucrose, lactose was not detected.  Hence, the presence of lactose in
  the plant kingdom should be re-examined.

"Is lactose really present in plants?" Takahiro Toba, Satoshi Nagashima, Susumu Adachi First published: 1991 https://doi.org/10.1002/jsfa.2740540217
So at least this possible source of lactose in plants is disproved.
EDIT: I also searched Web of Science for "lactose AND plant*" in the title field, and there are no articles other than the one @Remi.b found.

This isn't really an answer to your question, being merely a refutation of one source. However if you will post it do NOT post the quotation as an image, but take the trouble to type it out. Images of text are not indexable and discriminate against people with sight defects.

@David Two excellent points, edited accordingly, thank you.


text:
Identify this larvae that lives on a musrhoom?
I was in the forest near the Rhone river in France and I uncovered some mildewy wood bracket fughi (Ganoderma) on a fallen willow tree. It was a scene from a sci-fi film. some arthropod larvae of 2-3cm had built cocoons within a web, and the cocoons were empty and the larvae were wondering around on the mushroom.

Neat! Please update with location and approximate size of larvae and fungi. Thanks!

Thanks, added that info, Rhone Alps, France, 2-3cm. perhaps I have to take one captive in controlled conditions and see.

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text:
Cause of Obesity
Considering that the sequestering of 'persistent organic pollutants' [POPs] by adipose tissue is now established (see Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants by La Merrill et al. Environmental Health Perspectives, 121, 2013, pp162-169; pdf available here), is there any evidence that the existence of such POPs within fat cells interferes with the function of leptin, in particularly with the normal suppression of appetite in the hypothalamus?
Were there in fact such evidence, could such a derangement in leptin function account for tendencies to obesity in populations exposed to POPs?

The normal function of adipose tissue is to stare triglycerides. Please quote a source for your statement about organic pollutants (and for goodness sake don't abbreviate them as POPs).

It seems fairly well accepted that part of the function of AT is to store fat soluble toxins such as OPs. [e.g. Env.Health Perspectives 121(2) La Merrill]. There is a Korean study citing numerous references and discussing the relation of OPs to obesity [Obesity Reviews 18(2) Y-M Lee]. However, I could find no study which proposes an underlying mechanism according to which, presuming that the accumulation of fat serves an entirely necessary--rather than erroneous--function in all cases, dysfunction in the leptin-mediated circuit induced by OPs in AT is implicated. If so, it would explain a lot.

How do you differentiate between "function" and "they happen to accumulate there because they are fat-soluble? I thought it was the P450 system that had the function of dealing with toxic compounds, the endpoint being elimination (not sequestering). Whatever the connection between modern organic pollutants and obesity, you should remove the assertion that the normal function of adipose tissue is to sequester these compounds.

Perhaps it is more pertinent to ask to what extent fat cells discriminate between lipophilic organic compounds; the point being that because in the general case they do not, it is not unreasonable to argue--without quibbling over semantics or even raising the philosophical issue of intention--that this capacity for AT to dissolve, thus temporarily sequester organic pollutants within the process of their eventual detoxification--if this is indeed possible--, therefore protecting vital organs from the harmful action of these compounds. I will elaborate a little in answer to the question.

@user1136 That is good editing, and resolves some of the earlier objections to the question. I don't think my own answer which was effectively prompted by those unfounded objections in order to clarify that question deserves its down-votes by the way; since in the main what it states is correct, while contention about its latter paragraphs--which need not have been included but were-- is essentially a matter of opinion.

Leptin is the satiety hormone produced in the body fat cells - increased blood leptin levels suppress appetite and decreased levels stimulate it.
Persistent Organic Pollutants (POPs) are man-made chemicals that are environmentally persistent, leading to bioaccumulation in the food chain. Examples include polychlorinated biphenyls (PCBs) and polybrominated diphenylethers (PBDEs).
In the only study I've found that mentions the direct relationship between POPs and blood leptin levels, the exposure to POPs was associated with decreased leptin levels in women but not men: Expression of Obesity Markers and Persistent Organic Pollutants Levels in Adipose Tissue of Obese Patients: Reinforcing the Obesogen Hypothesis? (PlosOne, 2014):

Our study revealed a negative association between leptin serum
  concentrations in women, and the levels of several PCBs and BDE153 in
  both fat depots. Remarkably, in men, none of the analysed POPs
  correlated with leptin serum concentration.

In another study, the exposure POPs was associated with decreased levels of leptin in breast milk: Association between Several Persistent Organic Pollutants in Serum and Adipokine Levels in Breast Milk among Lactating Women of Korea (Environmental Science and Technology, 2015):

Leptin concentrations in breast milk were negatively associated with
  ∑hexachlorohexane (HCH), oxychlordane, ∑chlordane, or
  2,2',4,4',5,5'-hexachlorobiphenyl (CB 153) levels in maternal serum.

Both studies suggest, directly or indirectly, that persistent organic pollutants can decrease leptin levels and thus stimulate hunger, but the studies were small and are not, at least for me, considered sufficient evidence.

Excellent work.You understand the question, the possible importance of its consideration and have given a good informative answer. I agree that there is little evidence of the association, but continue to believe that it deserves more investigation. Naturally it would be difficult to establish a direct relation between POPs sequestered in fat cells and leptin function deriving in those cells; first it would be interesting to find if POPs are in fact present in fat cells of the obese. As you see, someone is so offended by my answer that he repeatedly down-votes it without proper reason.

@jeremiah, leptin is present in the fat cells of lean and obese people. I'm not sure how much the leptin levels fluctuate within the fat cells and if this has any importance, but it's the leptin that is released into the circulation that affects appetite in the hypothalamus.

@Jan.I know that leptin is produced in fats cells; the point of the question is whether the presence of POPs in the fat cells of obese people interferes with the conformation of leptin rendering it less effective at the H/T or even inert. The first question is to ascertain whether POPs are present in greater degrees in the fat cells of the obese than in a control group; and if not, whether they nevertheless exert a deleterious effect on leptin synthesis. If the leptin isn't working, then that's 'leptin resistance' isn't it. You're a young researcher aren't you? Well, there you are.

@jeremiah, from what I understand from the linked studies, the higher amount of POPs in the fat cells is associated with lower levels of leptin in the blood. I assume this is due to decreased release of leptin from the fat cells into the circulation. I have no idea if POPs affect leptin when there are still in the cells.

That's a start; and it may end up being the principal effect. I haven't yet read the linked articles; but I'll get to it. Thanks by the way for your effort in uncovering them. One of the reasons this is important is to establish some cause for leptin resistance which is associated with obesity; not necessarily so that it may be redressed, but at least that obesity might be better understood as a condition of 'leptin resistance', rather than a syndrome of grievous gluttony and sloth as it is often portrayed.

Leptin resistance would occur at the target cells in the hypothalamus. In this case, blood leptin levels would not be likely decreased. It's like insulin resistance occurs at the target tissue cells and the insulin levels are actually increased.

Yes, the inference of these studies is that POPs would not account for leptin resistance if they correlate with reduced serum levels. It seems we must leave the question unresolved for the moment.

It seems that the answer to this question is at present no--and might remain so until or unless researchers dedicated to elucidating any such relation between leptin and obesity are prepared to subject some population of poor leptin-producing creatures to given organic pollutants, with the aim of determining any measurable effect on leptin capability--a difficult assignment to say the least.
Various studies seeking to confirm the so-called 'obesogen hypothesis' have not unreasonably argued a mechanism of 'endocrine disruption' by certain common organic pollutants, but these are neither comprehensive nor capable of resolving certain paradoxes in the relation between leptin and obesity: notably that leptin levels are routinely observed to be raised in cases of severe obesity.  The idea of some derangement in leptin function induced by a local cause therefore becomes attractive in explaining such 'leptin resistance'.
At the same time, it is probably negligent to blame rising levels of obesity merely upon the delinquent appetites and profligacy of affluent people, particularly when certain benefits of fat accumulation, apart from the sheer simple joy of being fed, have been observed: putatively there are diminished rates of neuro-degenerative disorders such as Alzheimer's disease in the mildly obese. (There are various studies drawing such conclusions). Possibly such effects also pertain to the capacity for adipose tissue (AT) to sequester organic pollutants.
Now the respondent to this question has objected to the characterisation of this latter effect as a 'function' of AT when it is clear that this capacity for fat cells to accommodate fat-soluble substances without the necessity for their elaborate discrimination is indeed inherently and innately part of the broader function of AT.  The inference of the question itself is in fact that the proliferation of fat cells and fat mass in obese individuals may serve precisely this purpose or function.
Such an assertion requires no troublesome incursion into philosophical or teleological dispute--regarding ultimate cause or intention--nor great excesses of the imagination--that for example we are essentially organic creatures increasingly immersed in the products of oil and other hydrocarbons, themselves loosed from the ancient abeyance of that essential nature--, only the understanding that part of the actual mundane function of fat stores is to hold in continuing abeyance those organic compounds, in particular those which are broadly derivatives of hydrocarbons, which the organism generally is unable either to accommodate elsewhere in its metabolism, as if effectively indigestible food, or successfully to excrete.
It might be emphasised here that the aim of any such inquiry into the relation between organic pollutants and obesity--possibly mediated by a derangement in leptin function--is not of itself to redress any such local cause determined empirically; since realistically such would come only with the inevitable obsolescence of oil and the derivatives of hydrocarbons generally: petroleum, plastics, organic pollutants etc.
The aim is to elucidate the nature of this phenomenon of modern obesity, that at least it might be understood as part of universal necessity, that indeed it must in principle serve some eventual 'evolutionary advantage', not of a family of reproducing organisms--although this is an aspect of it--, but of the universal entirety itself in eternity (which some are emboldened by a peculiar philosophical perspective of the absolute inviolability of such a universal unity to characterise as the 'Unitary Soul', for want of a better description of the singular dynamic and process which must enliven it).
I might add here that there has developed an obsession in the biological sciences with a theory of evolution based not only on the philosophically repugnant idea of 'chance'--which despite the fervour with which such a paradigm is defended cannot of course be quantified in any meaningful way; which incapacity of itself requires that the entire notion be removed from orthodox thinking--, but on the necessity to impute to some detail of formal biological reality an evolutionary advantage conferred by such happenstance (e.g. in the usual view, base mutations) within some limited context, the niche, of which it is in any event merely an aspect, when the ultimate parameters of such advantage, more especially in the greater spatial and temporal context are essentially unknowable.
This is not to dispute the absolute preeminence of an 'evolutionary principle' within universal reality; only to argue that this principle is entirely singular and simply inherent within the fact of existence itself; and most importantly that the ultimate parameters of such a principle can never be objectively discriminated or 'known' by those such as we mere humans entirely immersed within  the mechanics of an inviolate universal unity in eternity. No conception of an ultimate 'evolutionary disadvantage' may be formed without the possibility for knowledge of the ultimate intention of such a dynamic universal unity.
And for those who would object that such an 'a priori' postulate of universal unity is improperly metaphysical in character, it would be well for them to remember that the existing scientific and cultural ethos of a blind aimless nature--Dawkinsism--, and the preeminence of 'happenstance' as its primary impetus--which is to say the denial of singular universal cause and intention merely for want of the capacity to discern it--, is only the expression of a passing alternative school of philosophy and its guiding paradigm, essentially that of 'chaotic erroneous nature' groping its cruel meaningless way aimlessly in the eternal darkness awaiting only the guiding hand of Man to render 'order' within it.

This answer is frankly terrible and one of the worst ones I have seen on this site. I would normally recommend adding references but I don't think even that can save it from all the illogical tangents and wrong statements. Universal unity? Unitary soul? A complete lack of any understanding of evolution?

@user1136. The reason for the post was to ascertain whether this was an original idea; since my suspicion is that it seems too obvious a connection not to have been conceived and studied previously; there were no references which I could find.  As such, the reference from a 2014 paper demonstrates that it is neither a novel idea nor without foundation, in spite of the previous reception of the question here. Moreover, there would seem considerable potential to investigate the idea that it is such a derangement in leptin metabolism which is at the root of obesity, if only to understand it.

Of course the hypothesis is unproven, nor have I supposed or stated otherwise; but I believe that part of the purpose of forums such as this is to air such ideas among those with the where withal and inclination to pursue them.  That latter part of my answer is intended only to express a particular philosophical perspective--just a form of old-fashioned determinism really, newly expressed--, the implication of which is that whatever mechanism is finally established for the effect that in the modern day, there are some who simply cannot satisfy their appetites, it is nonetheless an entirely..

..an entirely necessary and intrinsic part of nature: in this view nature, reality itself, simply CANNOT EVER be in error, regardless of how things may appear locally or temporarily. What appears as a error or deficiency in one aspect of a Unitary Universal Principle represents only the incapacity on our part to determine its greater context. Neither is this a new idea; anyone familiar with Schopenhauer for example, to cite a modern thinker, knows this. However, in modern times, the implications of such a view are far more troublesome to an ethos of scientific manipulation than previously.

@BryanKrause. The gulf between our views is probably too great to bridge here; however, since it is essentially philosophical, I would humbly request that you regard it as such.

The answer is carefully written to separate the quite plausible rational if also arguable idea that some recent modern influence apart from the ready availability of KFC etc. might be responsible for what is undoubtedly an epidemic of obesity in Westernised societies--for example, some disruption in leptin function which may at the same time amount to the establishment of an evolutionary advantage in dealing with POPs--, from the later expression of a philosophical view of the circumstance itself of such a condition.That view does not deny the operation of an evolutionary principle, for what..

..for what other reason does reality exist? It simply conceives of that operation in another way. It does not for example understand base mutations to be other than orderly transitions in the configuration of DNA conforming to the exigencies of that principle which indeed also tend to preserve the basic structure of that genome. Nor does it separate organism and niche in the ordinary way;affording a much greater importance to epigenetic function, and therefore to the heritability of genetic potential, thus 'adaptability' which is inseparable from the memory of environment continuous with it.

So, I suppose what I'm trying to say is that while I can appreciate the traditional theory of evolution, I simply cannot accept it philosophically; and am therefore compelled to take a broader view; which happily leads to what I find to be a more satisfactory explanation of phenomena, and of the intricacies of empirical observation; in particular the structure and function of DNA, and its dynamic of replication and transcription. Eventually, the underlying physics itself of that dynamic will be demonstrated to conform to that of a 'unitary universal wave principle' operating ubiquitously.QED.

@jeremiah I think you misunderstand the purpose of this stack. It is not to propose philosophical ideas, but rather to answer specific questions with referenced, scientific answers.

@Bryan Krause. With respect, sometimes an answer requires a different philosophical perspective, particularly when the principal foundation of the traditional answer is merely a prevailing philosophical view. At the same time, it is not my intention here to expatiate thus.In this case, a good well considered question was asked and because it was roundly derided, I answered it myself in the hope of elucidating the idea. As you now see, there is good evidence that the idea has merit. I do wish therefore that you would please not continue to attack this and other questions; rather answer them.


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Identifying a mushroom (Switzerland)

Does anyone know this type of mushroom? It grew during the last week in large numbers in one of my pots on the balcony, location Zurich, Switzerland. A smaller part of the soil is from the wood in the neighbourhood, so it might have originated from there.
I spent some time researching on the Internet, and think it might be related to the Armillaria family. An expert opinion would be very much appreciated.


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Identification of a young tree in the alpine region of southeastern France
I have a young tree growing in my backyard (in Grenoble, France), and I was not able to identify it, despite searching with many identifier tools.
It's 2 years old now and must be 2 meters high. It has a grey trunk, its leaves grow on brown/red stems that protrude irregularly from the trunk.

The leaves are pointed, gently serrated, covered with a light fuzz, with a distinct lattice of veins.

Could you help me identify it?

This reminds me of "lilas" (Syringa): http://www2.csdm.qc.ca/st-fabien/projets/arborophile/Lilas/lilas.htm I'm not at all confident about the identification, though.

I have a lilas nearby, unfortunately they do not look alike. The lilas leaves are smooth and go two by two. Sorry for taking so much time to reply. The tree is still growing really fast, some of its leaves are huge, but there is still nothing more to help identification, no fruit or flower.

Could you add a photo with a zoom on the connection between a leaf and a branch?

The tree grew its first fruits this spring, so that I could definitely identify it: it is a goat willow! This is consistent with its spontaneous sprouting in my yard, as it is a common tree in my region.


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What kind of beetle has fuzzy orange antennae and can flip its head down for digging?
Some years ago I found this beetle while hoeing potatoes in Iowa in the United States. It had something like branches on its legs and could bury itself out of sight in five seconds! If I recall the beetle itself was mostly black.  It had the ability to flip the front part of his body up to reveal the face which was normally down facing the ground. I suppose because it usually lives underground. But when it flipped its head up, it's antennae came out and were bright orange, fuzzy ,and had round ends similar to an old-fashion side mirror on a car. When it's head was down it had a horn almost like a rhinoceros beetle.  But when it flipped its head up it had buggy eyes - the cutest little face.  I have never been able to find out what this little critter was. I just ran across my description of it in my journal today and tried to look it up online, finding your website.  Sorry, I didn't own a camera back in 2000 to take a picture of him.

I'd guess that the beetle you found was of the genus Nicrophorus ,family Silphidae . They are commonly known as Burying beetles and are true to their name
was this the beetle you saw?


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Why are prokaryotic promoter sequences written 5' to 3', when transcription proceeds from 3' to 5'?
It seems that the promoter regions are written from the 5' to 3' direction. My lecture notes, for example, give the -35 and -10 promoter regions sequences like so:

Wikipedia seems to agree, on their article about promoters.
However, RNA polymerase transcribes in the 3' to 5', as in  it reads the template strand in the 3' to 5' direction. In that case, why aren't the promoter regions written also in the 3' to 5' direction?
Meaning, instead of the -10 sequence being 5'-TATAAT-3', why is it not 3'-ATATTA-5', in agreement with the direction of transcription?
My intuitive guess is that the $\sigma$ factor recognises the promoter region in a 5' to 3' directionality. But I cannot find any information to back up this guess. Additionally, if this is true, how could it have been determined (experimentally)? Furthermore, whatever the answer is, does it also apply to transcription in eukaryotes?

Possible duplicate of What direction is a sequence in databases written?

Come on. You can't have people driving on the left in one town, and driving on the right in the next. It's bad enough when us Brits go on the Continent. There's no mystery, we just read all gene features on the same strand.

@David Fair enough, I'll take it as a consequence of convention. Thanks!

DNA sequence by convention is written starting at the 5' position so the directionality is assumed without explicitly writing the 5' and 3'. As for why its not the template strand sequence. I would say that's also a convention for simplicity because you only need to write one sequence if you want to discuss genes and regulatory elements.


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With respect to which METRIC is my DNA 99% similar to any other person's DNA?
I clarified my question, by editing the title. Using the comments  and links below, I have answered it myself:
The answer to my question is: The similarity is between 98.4%-99.9%, depending on which type of differences you include. The numbers relate to writing my and the other person's DNA as a long string, and compare differences (change of letter, missing/inserted letter). The most important differences seem to be SNPs (=difference in a letter in a gene-coding sequence) and account for 0.1% of difference between our 2 DNA's:

http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=110248
http://book.bionumbers.org/how-genetically-similar-are-two-random-people/

I have striked out the original question text, because it includes some motivation and interpretation, which seems false.
edit: It was suggested that the question is a duplicate to "Same" DNA vs genes but this might seem not to be the case, as this question just concerns the used metric (compare answer below).

99.9% vs 88%:
2 person's DNA is 99.9% the same (which goes down to 99% in some sources), e.g. http://book.bionumbers.org/how-genetically-similar-are-two-random-people/
Does this number include differences in copy-number variations and maybe other ?
On the other hand https://www.nature.com/scitable/content/global-variation-in-copy-number-in-the-13571 says that there may be up to 12% of some other differences (I am not sure what those differences mean).
Question:
I have been pouring through the internet and books, but have not yet understood to which metric this 99.9% number refers to? (I am a pure mathematician)
My hypothesis what it means:
If we look at a 1000 base-pair long snippet of the DNA of person A, then we will find this same snippet somewhere also in person B's DNA, with just one difference in one of the 1000 base pairs.
Now, if the latter is true, then this means that my DNA may still be significantly different than my neighbours, e.g. by containing a different number of repetitions in the non-coding DNA.
Ultimately, my DNA could be only, say, 2% similar instead of 99.9% (depending on the number of different repetitions), if we used as a metric the number of single base changes (including single deletions/insertions), we need to do to go from the DNA of person A to the DNA of person B (assuming we wrote down each other's DNA in one long string). Question 2: In fact, I would be quite interested to know how much the DNA of two people is similar using this last metric?

Please quote the exact passage in the Nature paper which you think says that there may be 12% of other changes. I have looked at the paper, searched for "12%", and all I can find is the statement " A total of 1,447 copy number variable regions (CNVRs), which can encompass overlapping or adjacent gains or losses, covering 360 megabases (12% of the genome) were identified in these populations." If you think that this meanss that individuals differ by 12% you are mistaken and your question is based on a false premise and should therefore be withdrawn.

@David Thanks for the comment. My question is fully independent of the 12% number, so withdrawal may be a bit too much. I use the number in my motivation. You may be correct that I misunderstood, because the sentence you mention is the one I am referring to. Compare also the BBC-article http://news.bbc.co.uk/2/hi/science/nature/6174510.stm - my misunderstanding possibly reinforces the need for an answer to my question: Which metric are we talking about? If you have some explanations or links/books, that can give me a better understanding, I am happy to learn as I have little clue right now :)

The 99.9% metric is quite straightforward — a simple base for base comparison between two DNAs — and is dealt with in my answer to this question. If you want to analyse something different like gene duplications (as in the paper you cite) you need to understand the biology and devise your own metric. Any paper with such in it will have it defined (possibly in the supplementary material.


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Measuring gene similarity in two bacteria models
I'm currently working with some computational models of bacteria. The bacterium I am considering is an Ecoli K-12 which has 139 genes. I have several models of the same bacterium with different combinations of genes that are active. e.g. M1 - M3 are the models and G1 - G4 are the genes. 1 indicates the gene is active and 0 inactive.
M   G1 G2 G3 G4
M1  1  1   1  1
M2  1  0   1  0
M3  0  0   1  1

My assumption is that bacteria have a fixed number of chromosomes and randomly genes get activated. I intend to compute a similarity score between each pair of models (how similar two models are). I want to know what similarity means in terms of biology. Is a gene being active (1) considered a similarity or begin active and inactive (1 and 0)? For example if I compare M2 and M3 which similarity would be correct?

1 similarity (only G3 is active)
2 similarities (G3 is active and G2 is inactive)

The word "bacteria" is the Latin plural of "bacterium". I have corrected this. However I find your question very difficult to understand. When you say the bacterium has 139 genes do you mean that you are considering 139 of the several thousand in E.coli? And as far as I can see, the genes are always present in the genome (which, incidentally, is a single circular chromosome), so if you modelling activity you cannot talk about present and absent, but need to use terms like "active" and "inactive".

@David Thank you for the edit. Yes you are correct. I should have made it clearer. The model simulates only the metabolic activities in the E-coli. Therefore the genes are the ones that are related to the metabolic pathways. Also I think active and inactive should be the proper terms.

I feel like you could look at this in terms of local and global features. In other words, sets of active/inactive genes that are part of their own module versus the overall set of active/inactive genes. You could also look at pairwise comparisons ({M1,M3} {M1,M2} {M2,M3}), or define a reference/wild-type to compare all other models against (as in differential expression, M1 vs. M2, M3... Mn).

It may not be correct but if it were me, I'd look at M2 and M3 and say they are 50% similar because half the genes broadly "match". Something like "they have 2 similarities" seems odd to me.

@CKM thank you for your comment. What I meant by 2 similarities is that they are 50% similar. Also I think computing the % activity is also a good idea. Thank you.


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Why there are no plants that offer salt fruits as opposed to sweet fruits?
Why there are no plants that produce salt fruits?
Is it because other animals do not like salt to the same degree of humans?

If you could mark the question as answered that would be awesome! :)

Soil salinity and sodicity cause severe problems in agriculture worldwide, and salt tolerance in crops is an extremely important trait and a major focus of research. Detrimental effects of high salinity on crops are multifaceted and affect plants in several ways: drought stress, ion toxicity, nutritional disorders, oxidative stress, alteration of metabolic processes, membrane disorganization and reduction of cell division and expansion (Hasegawa et al. 2000; Munns 2002; Muscolo et al. 2007, 2013; Zhu 2007; Sidari et al. 2008). As a result, plant growth, development and survival are reduced (Muscolo et al. 2011; Schleiff and Muscolo 2011). Two major stresses affecting plants under salinity are osmotic and ionic stresses. Osmotic stress, occurring immediately in the root medium on exposure to salts, can result in inhibition of water uptake, cell expansion and lateral bud development (Munns and Tester 2008). Ionic stress develops when toxic ions (e.g. Na+) accumulate in cells causing increase in leaf mortality, chlorosis, necrosis and decrease in the activity of cellular metabolism including photosynthesis (Yeo and Flowers 1986; Glenn and Brown 1999). In fact, excess Na+ and Cl− have the potential to affect plant enzymes, resulting in reduced energy production and other physiological processes (Larcher 1980; Morais et al. 2012a,b). Ionic stress results in premature senescence of older leaves and in toxicity symptoms (chlorosis, necrosis) in mature leaves due to high Na+ and Cl− which affect plants by disrupting protein synthesis and by interfering with enzyme activity (Munns and Termaat 1986; Hasegawa et al. 2000; Munns 2002).

Source: Effect of saline water on seed germination and early seedling growth of the halophyte quinoa
Salt is really good at inhibiting enzymes and biochemistry, which translates into not being great for seeds. So to have a fruit that has a high concentration of salt is really risky and not likely to be successful. Sugars on the other hand attract a multitude of other organism that would help move seeds around or create an ideal growth environment. To have crops that are resilient to salt would be useful but would require a lot of wasted energy to maintain osmoregulation. So it's not so much that animals wouldn't eat a salty fruit but more that it would be harmful to the seeds.

Also the only places where salt is common enough for plants to stuff their fruits with it are the very places animals do not need more salt as they can get plenty from the environment.


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Effect of high temperatures on plant stomata
My biology textbook states that stomatal closure occurs at high temperatures to avoid water loss. Another stackexchange thread I can find (What is the effect of temperature and carbon dioxide on the opening and closing of stomata?) agrees with this, however most actual studies on the subject I can find talk about stomatal opening occurring at higher temperatures, but say the effect if the plant is experiencing water stress.
Does anyone know why there is conflicting info on this, and which source is correct?

I wondered the same. According to biology lectures I had stomata cells are opened by turgor (water pressure within cells). There are several depicted mechanisms. In some illustrations there is like a lid sitting on top of the stomata and turgor opens the lid by pushing it upwards. In other turgor deforms the cells so that they form a hole between them (a stomata). According to this theory as long as there is enough water available stomata should remain open, but probably other mechanisms exist.


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seafood muscles - how do they work?
Today, first  time in my life I ate seafood. It was a squid and a calamar. Note that I am biology layman, so please be merciful :(
While dissecting my food I noticed that the tissues of those creatures were homogenous white mass. Completely different than with pork or chicken, where you can easily see the directions of muscle fibers and different groups of muscles. Just looking at a chicken wing tells you which muscle does what.
But why are squids and calamars so homogenous? How is it possible they work? Why is it like that?

As far as I know, the squid's mantle has two layers of muscle, circular and radial muscles, and two layers of epithelium or "tunic." This is unlike animal muscles, where the parts we eat are striated skeletal muscle. The mantle would be more akin to intestinal tissue with circular smooth muscle I'd imagine. That's about all I know, though.


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What species is this mosquito-like insect?

I found this in my room in Serbia. It's not a local type of mosquito that I'm familiar with, so I'm very interested. It flies like a fly but it looks like some kind of mosquito. I am looking forward to seeing what this could be.

Where are you from? could help track it down

I am in Serbia, Europe. :)

This is a dance fly, family Empididae (broad sense; two or three groups are extracted for the narrow sense), but beyond that I can't go (I don't have the Palaearctic identification keys).  If you were in North America I'd be halfway confident calling it a species of Empis, but there are a lot of them (and the genus is also found in your neck of the woods).

Wow,thank you so much,it looks like this is it :)

@ArthurJFrost You could make an answer out of your comment.

@Arthur I think Empis is not unlikely in Europe too.

@Remi.b, I'd prefer not going further than I have already; as I said on May 1 there is information I'm missing, and it's possible that even if I had it, the photograph here might not be detailed enough to use it (the key for this group in Manual of Nearctic Diptera, volume 1 [see the Entomological Society of Canada website; they have that in PDF] require at least a stereoscope for effective use, even when the animal is fairly large).

@рüффп No, the text is about Russia. But in Russian Russia is written Россия. In Serbian and in Macedonian it is written Русија. Due to its wast territory, providing Russia as location wouldn't be very helpful.

@ArthurJFrost well, you've clearly established yourself as a knowledgeable entomologist on Bio.SE, so it's fairly doubtful others will be able to provide a better answer (without themselves having the appropriate key). I think providing a write-up detailing the family would be a more than acceptable answer here. You could "improve" the answer by discussing typical characteristics to look for to identify genera/species in this specific family and possibly a citation/link/title to a potentially useful key. Sounds like a comment about Empis is warranted here, too.


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Help identifying leaf-like bone
I found two of these objects near a creek in Missouri. They feel like they are made out of bone but they do not look like any bone I have seen before. They also appear as though the could be some sort of plant part. I am having a very difficult time identifying them and any help would be appreciated.

Those are isolated turtle bones:

Specifically, they are part of the carapace, or upper shell. The projections would articulate with the backbone. The "toothlike" structure at the other end projects down toward the margin of the shell.
Based on the size, and the fact that you are in Missouri, I'm guessing they are snapping turtle bones. Here's a photo of the inside of a snapping turtle shell:

They are a little hard to make out, but you can faintly see the marginal projections.

These are, as stated in @kmm's well-received answer from 2 years ago, osseous components of a turtle's carapace, or upper shell.  More specifically, these bones are called pleurals and consist of the turtle's ribs surrounded by "fused dermal tissue" [Wikipedia]. From Wyneken (2001):

Each rib head is aligned with the junction of two vertebral bodies (Fig. 91). Fusions of vertebrae and ribs with dermal bone result in unique carapacial bones...pleurals are formed by the ribs and their dermal expansions...(Figs 92...)

 Fig 92b (left/top) and Fig 91 (right/bottom) from Wyneken (2001) showing pleural bones and rib heads articulating with vertebrae. (Illustrated by Dawn Witherington)
The projections you see sticking upward off the table in your final photo are the rib heads that would articulate with the turtle's vertebrae.

Fun facts:

Obviously, the fact that their ribs are fused in this way to form the skeletal component of their shell means their ribs do not move during ventilation as seen during "costal ventilation" in many other vertebrates. Never worry; they use a unique ventilatory apparatus involving hypaxial muscles to achieve ventilation instead. See Lyson et al. (2014) for more.

So what is the benefit of having broadened ribs? Protection, right? Well, maybe not... Lyson et al (2016) believe that fossils of early turtle ancestors suggest that ribs first broadened to provide an "intrinsically stable base on which to operate a powerful forelimb digging mechanism" to allow early turtle ancestors to live underground.

Citations
Lyson, T.R., Schachner, E.R., Botha-Brink, J., Scheyer, T.M., Lambertz, M., Bever, G.S., Rubidge, B.S. and De Queiroz, K., 2014. Origin of the unique ventilatory apparatus of turtles. Nature communications, 5(1), pp.1-11.
Lyson, T.R., Rubidge, B.S., Scheyer, T.M., de Queiroz, K., Schachner, E.R., Smith, R.M., Botha-Brink, J. and Bever, G.S., 2016. Fossorial origin of the turtle shell. Current Biology, 26(14), pp.1887-1894.
Wyneken, J. 2001. The Anatomy of Sea Turtles. U.S. Department of Commerce NOAA Technical Memorandum NMFS-SEFSC-470, 1-172 pp.

@Downvoter, why the down vote? Please let me know if you see something that I need to edit. Thanks.


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How to determine which is the nucleotide sequence of a gene?
I have came across a few  genes that show different nucleotide sequence in different databases. I then found out that the sequences are actually reverse complement of each other. How do i determine which is the actual nucleotide sequence of a gene,and not the reverse complement version of it?

Usually the reported sequence for a mRNA in NCBI is the sense strand. Can you give an example of a gene whose sequence you are unsure of?

Possible duplicate of What direction is a sequence in databases written?

Hi @WYSIWYG below are the nucleotide sequences of the rplC gene. The first one is from NCBI, while the second I received from a sequencing company for my strain:

ATCC 19977 R rplC ncbi
CTACTTCTCACCTCGCTTGACAGCGGTGCGGACCACAACCAAGCCACCCTTACGTCCGGGGATGGCACCC
TTGATCAGCAGTACGCCGTTCTCGGCATCGACCTTGTGCACCACCAGGTTCTGAGTGGTGACGCGATCGC
TACCCATACGTCCGGACATCCGGGTGC
M61 S
ATGGCAAGAAAAGGAATTCTGGGCACCAAGCTGGGTATGACGCAGGTGTTCGACGACAAC
AACCGGGTTGTCCCGGTAACCGTCGTCAAGGCCGGCCCCAATGTGGTGACCCGCATCCGG
ACCACCGAGCAGGACGGCTACAGCGCCGTGCAGCTCGCGTATGGCGAGATCAGCCCCCGC
AAGGTGACCAAGCCGGTCACCGGTCAGTTCGCCGCCGCGGGC

It's really important for me to know the exact sequence, as i am looking for a nucleotide change at a specific location

You run a blast of your sequence. Then explore the results and you'll see somewhere that says "strand"  and is indication whether is plus/minus.
https://blast.ncbi.nlm.nih.gov/Blast.cgi
Also blast has a graphical interface in which you'll clearly see the matching and non-matching bases. Therefore it should help you to identify the differences between the 2 sequences.

In general, if you look up a transcript sequence it will be in the correct orientation.  If you look up a gene based on genomic coordinates, it may not be.
We can't tell you why your first sequence is in the wrong orientation from what you pasted.


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Why are not both alleles knocked out at the same time in knock out mouse?
I was reading this little 'article' about homologous recombination and knockout mouse. According to this article you first remove embryonic stem cells from a gray-fur blastocyst, then insert the construct and place them back into the blastocyst. Further the text states:

A knockout mouse has had both alleles of a particular gene replaced
  with an inactive allele. This is usually accomplished by using
  homologous recombination to replace one allele followed by two or more
  generations of selective breeding until an breeding pair are isolated
  that have both alleles of the targeted gene inactivated or knocked
  out.

However what I don't get here is that we have cells from an embryo, and thus have cells with both alleles. Hence, the regions surrounding these alleles will be homologous, so why would this step result in heterozygous (and thus require selective breeding afterwards) instead of homozygous mouse direcly?

It is a simple matter of probability. If the probability of replacing one allele is p then the probability of two alleles getting replaced would be p2 (note that the latter will be smaller because probabilities are less than one).
If you have a selectable marker such as GFP then you'll end up selecting both heterozygotes and homozygotes but the frequency of the former will be much higher especially when you consider the fact that the probability of homologous recombination mediated knock-out/in is very low in mammalian cells (10-7 – 10-5). Therefore, inbreeding is an easier way to obtain homozygotes than screening the ESCs. Moreover, selective breeding is inevitable because in the first round will just produce chimeras (not all ESCs are replaced with the modified ones).
Technologies like CRISPR are now being used to accelerate the rate of gene replacement.

Thankyou, I have one additional question. Why would you not just replace all ESCs? Or is this simply not technically possible?

@RickBeeloo It would be very challenging. Almost impossible.


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Are releasing-hormones and release-inhibiting hormones from the hypothalamus ever present in the blood?
Our teacher said that these two hormones are normally never present in the blood stream, and to be carfeul of it if it comes as a question. I'm not conviced to be honest, is this true?

I think your teacher means that these hormones only go from the hypothlamus to the anterior pituitary gland, where they stimulate hormone secretion. Like, for example, of the FSH or LH, who are stimulated by GnRH. GnRH is not present in the systemic sirculation, but it's definately present in the one between the hypothalamus and the APG. FSH and LH are though. I don't remember the name of the small blood-system between the hypothalamus and the APG, but I don't think it's connected to the systemic circulatory system.

Yes that was what he meant, he said that if one did a blood test and took blood samples (from places like the viens of the arms , like normal) you wouldnt find these hormones.

I would think it's true, but if you just google whether the different blood systems (systemic VS hypothalamus-APG) are connected you have your answer.

I see. Thanks, I didn't know the name of that system. I'll google it and see what I get.

https://en.wikipedia.org/wiki/Hypophyseal_portal_system got it!

This isn't strictly true. The hypophyseal portal system, like other portal systems (e.g., the hepatic portal system), is part of the systemic circulation, but has a second capillary bed. Releasing hormones act at very low concentrations. They are released in a pulsatile manner and are inactivated by enzymes in the blood, providing tight control of their activity in space and time.


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How does the Lgr5 receptor contribute to maintaining stemness in the intestine?
I don't understand the connection between Lgr5 receptor and Wnt between Paneth cells and stem cells. And how does this link to the EphB-EprinB inhibition between transit amplifying cells and differentiated cells?
My book "The molecular biology of the cell" 6th edition (Garland Science) only states that the Lgr5 receptor in the stem cells makes them able to create a mini-gut (organoid), but I am asked to present factors that makes the gut able to totally renew itself and maintain its structure.
I have already answered the Delta-Notch lateral inhibition pathway and its connection to Wnt signaling from the paneth cells in determinating differentiation and maintaining in ability to divide.


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When was it understood that a male haemophilia sufferer can't pass it on to his sons?
Haemophilia A and B are both X-chromosome mutations, so a sufferer necessarily inherits the disease from his mother. She won't have serious symptoms unless both of her X chromosomes have the mutation, which is very rare. Since sons of a sufferer necessarily inherit his Y chromosome, they can't inherit the disease from him.
I'm trying to find out when it was understood that sons of a sufferer could not inherit the disease from their fathers. The relationship between chromosomes and heredity was clearly demonstrated in 1915. The idea that females were usually carriers and sufferers usually male had been understood since 1813. The XY sex-determination system was discovered in 1905.
However, it is not clear to me when this would all have been put together and become part of normal biology and medical courses. I think the crucial points are:

There are sex-linked genetic conditions.
Haemophilia is one of them, and is an X-chromosome recessive condition.
Men are XY, women are XX.

Can anyone help with when all of that became normal knowledge for doctors and biologists?
Titles and authors of biology textbooks from the 1920s to 1945 would help, since I'm quite prepared to seek out old books, if I know what to hunt for.

This page might give you some clues to follow up.

@David: Sadly not, but it has shown me how my question was unclear, and I've improved it.

Sorry about that. Chasing up these historical things is very time-consuming because there is so little on the Internet, which is in any case obsessed with the latest thing. I just wonder whether you would have had to understand the XY sex-determination system to draw the conclusion about non-transmission to sons.

Thanks for trying, it was worthwhile. Understanding XY sex-determination means you know non-transmission to sons is basically impossible, rather than just unobserved. This is for a story set in the 1940s, and the question is if it's possible to be sure that a sufferer isn't the son of someone known to be a sufferer.

Using Google Scholar, I've found the oldest publication on this item.
1911 - "The pathogenesis of hereditary haemophilia".
In this article you'll find a complete synthesis of all the works done about haemophilia till 1946.
OP adding a summary, in case of future link rot: The linked article is from 1946, based on research in the late 1930s and early 1940s into the statistics of haemophilia. It's attempting to estimate the mutation rates of X chromosomes in males and females, and to test if X-Y crossover allows the haemophilia mutation to skip generations. It assumes the knowledge that leads to the conclusion that a male sufferer can't pass it onto his sons.


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What is this apple's abnormality?
The apple pictured is a of the Gala variety,typically striped.The stripes swirl around a brown protrusion. The protrusion is flexible,in the way a leaf is flexible. The flesh underneath is not discolored or soft. The apple is not misshapen,the seeds are not un-developed or underdeveloped. What is this brown protrusion called and what causes it?

Did it grow on/next to a branch?

I don't know. It was sold loose it a supermarket. I only saw it after it was picked.

I take it that the question is about the mis-shapenness of the apple, that the stick we see in the dip is the core. The morphology (shape) of fruits such as apple and pear are very sensitive to how well the fruit was pollinated. As we know there can be a variable number of seeds in an apple, but the important fact determining shape is that there should be viable seed develop in each of the five seed pockets resulting in balanced development of the fruit. If the pollination is poor and only a few embryo seeds are fertilized, then the development of the surrounding flesh will favour the pockets that contain viable seed, resulting in possibly mis-shapen fruit. Once you have wondered enough and decide to eat, cut open carefully and on the small side you should see that the seeds are either too few, non-existent or failed to develop.

Not sure what you mean "the stick we see in the dip is the core".  I have seen this odd thing few times before on apples, but usually a little less extreme than in peter's picture. In the ones I have seen, the apple isn't really mis-shapen. It just has a small flexible, as peter calls it, "protrusion" on the side. The structure inside the apple seems completely normal, and the stem, core, and seeds look fine. I think this little blemish is really just a surface phenomenon. ...However,  I certainly don't know what it is or what causes it, so I am curious to see if there are any other answers.

Thats right, Lorel C. My question is about the brown thing on the side of the apple, not misshapeness.

I don't know what part of the tree it grew on.It was sold loose,in the supermarket.


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What does "Origin" mean in NCBI GenBank?
I'm having trouble determining what exactly is meant by the term "Origin" in this case. It is just before a 70 bp sequence that the page claims is a plasmid, but does not specify it to be what I assume is incomplete, seeing as I don't think there is such a thing as a 70 bp plasmid (correct me if I'm wrong). So do they mean the origin of replication to the plasmid?
Here is the page in question: https://www.ncbi.nlm.nih.gov/nuccore/M30888.1?report=genbank

The ORIGIN may be left blank, may appear as "Unreported," or may give a local pointer to the sequence start, usually involving an experimentally determined restriction cleavage site or the genetic locus (if available). This information is present only in older records.
The sequence data begin on the line immediately below ORIGIN.

[source]
Given that it's left blank in your file, it doesn't signify anything other than the end of the annotation and beginning of the raw sequence.


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Would this disprove the theory of evolution?
I did my philosophical homework today in which I answered the question of whether evolution could be disproved.
I basically argued that one way it could be disproved was if one could prove that humans are somehow "perfect" (see below for definition) and for which the probability of evolving by natural selection was 0. This would mean that evolution could not explain the existence of humans in nature, and so natural selection would be disproved. While this is philosophical, the reason I posted it on here is because I am not a biologist, and am rather interested in what biologists would make of this idea, and whether it is just complete nonsense (which, not being a biologist, I do not deny).
My definition of "perfect" was that it would have to be mathematically proved perfection. It would be no good to just say humans can do mathematics while other animals can't, therefore humans are perfect. This is too vague. So I defined something as being "perfect" if it was proved mathematically as being perfect. I defined this as being done by a new "mathematics of consciousness" which would then be applied to different animals, and only humans would come out as being perfect according to this (as yet undiscovered) mathematical theory. And then one would have to show that the probability of this occurring via natural selection was 0.
Edit: a more precise example explaining how evolution could be disproved (to avoid ambiguity):

Describe consciousness mathematically
Show that, for humans, this shows up as something similar to the Riemann Hypothesis, where all the zeros lie on one line.
Show that this cannot occur via natural selection, either due to the infinite amount of time needed, or because of corruptive influences in nature, etc. The point is that the probability would be 0.
This would imply that natural selection is inadequate for explaining humans.

This proposal doesn't really make any sense scientifically especially because you are starting from a premise that doesn't make any scientific sense: "mathemetically proven perfection"

@BryanKrause: Thank you for your response. Could you please elaborate what is wrong with there being developed a mathematics of consciousness, which somehow shows that humans are "perfect"? As I said, I am not using "perfect" vaguely, but rather in the sense that when this mathematics is applied to humans, it would show that the probability of this occurring via natural selection was 0. This could be something like showing that all their "zeros" (which would have a definite meaning in this new mathematics) lied on the same line kind of like in the Riemann Hypothesis for example.

@Raghib: This fails because 1) There is no universal definition of "perfect"; 2) Why should consciousness be an aspect of your ill-defined perfection.  Tardigrades and cockroaches are superior to humans in many respects, and are probably not conscious; 3) The fact that humans are imperfect is practically demonstrated by the vertebrae of my lower back, among many other things.

I'm voting to close this question as off-topic because it is not a question about Biology in terms of SE. This is a clear discussion question about, as the poster admits, philosophy. That falls clearly into the sort of questions one should avoid asking.

I agree that it's off-topic.  Still, I'm a bit curious to know which individual human might be considered perfect, since no two of us are identical.

Humans are far from perfect by any definition, the human body and mind are full of recognizable flaws, everything from poorly designed eyes, anuses, and backs to minds that see faces and minds where they don't exist.

Your revised question contains a fundamental paradox.  If your #3 is true, then #4 follows, but the logical consequence of that is that consciousness can't exist.  That is, either humans became conscious through natural processes, or they were created by some entity that supplied consciousness.  But that entity must have attained consciousness through some natural processes, which by #3 can't happen.

What do you mean by "Darwinian evolution"?
The theory of evolution (aka. modern evolutionary synthesis) is much more than what Darwin said in his books. Calling it "Darwinian evolution" is misleading (and is very rarely used in the scientific literature).
What is the theory of evolution?
The theory of evolution represents a large set of tested hypotheses. It does not mean much to disprove the theory of evolution, as much as it would mean something to disprove specific elements of this theory.
Would "showing that humans are perfect" disprove an element of this theory?
I don't really understand the hypothesis that you are willing to be testing. It is unclear how you define "perfect" and what you mean by "mathematics of consciousness". All these concepts are very undefined. If they are clear to you, please define them and please suggest a clear experimental set up and we could talk about it. You also seem to phrase your hypothesis upon an explicitly undefined mathematical tool (according to this (as yet undiscovered) mathematical theory). That makes your hypothesis very unclear.
In any case, stating that it would be the only way to "disprove the theory of evolution" would be extremely wrong.
How to disprove specific elements of the theory of evolution?
There are millions of ways to disprove elements of the theory of evolution! There are maybe ten thousands (maybe more, maybe less, I don't know) papers published every year in the field of evolutionary biology. Many of them, to some extend, are opportunities to test falsifiable hypotheses about the modern evolution synthesis. For examples

show that a beneficial mutation that sweeps to high frequency does not reduce polymorphism and heterozygosity at linked sites.
show that new living organisms are being created spontaneously
show that fossil age estimates through carbon 14 and other methods do not match estimates with molecular clock.
show that mutations don't happen.
show that any functional (such as beneficial mutations) or structural (such as gene duplications) subcategory of mutations do not happen.
show that the probability of fixation (fixation = reaching a frequency of 1 in the population) of a mutation associated with a given selection coefficient does not depend upon the effective population size.
show that a lineage cannot evolve reproductive isolation
show that there is no genetic variance in populations
show that coalescence times don't differ among independently segregating sequences.
show that allele frequency do not change in experimental evolution experiments
show that population selection does not work in experimental evolution experiments
show that fitness heritability is zero
etc...

Your essay
It is funny that such question is being asked to you in a philosophy class. One can only suggest falsifiable hypotheses if (s)he understand the underlying set of claims to be challenged. I understand that the purpose of the essay is likely to get you more familiar with the concepts of falsifiability but the students might miss the science skills required to investigate the question on a given specific scientific theory. I suppose that if you were asked the same question about the theory of strings, you might realize better that it does not take a philosopher to produce such hypotheses but a physicist. At the end of the day, addressing the question in this essay would require you to learn a bit more about evolutionary biology.
About your edit

Edit: a more precise example explaining how evolution could be disproved (to avoid ambiguity):

Describe consciousness mathematically

This remains to be done. One cannot ask whether a test makes sense without defining the concepts being tested. It is like asking I would like to test if schmilblik equals 3. First, we'll need to define schmilblik. Would this disprove Newton's theory of gravitation?. One cannot tell whether it would disprove Newton's theory of gravitation without knowing what the schmilblik is! Whether it disproves anything depends upon the definition of schmilblik.

Show that, for humans, this shows up as something similar to the Riemann Hypothesis, where all the zeros lie on one line.

I am not really familiar with Riemann Hypothesis so I don't really understand what you mean here, sorry. Also, I am not sure what zero would mean on your scale of consciousness!

Show that this cannot occur via natural selection, either due to the infinite amount of time needed, or because of corruptive influences in nature, etc. The point is that the probability would be 0.

I am not sure what "this" is in your sentence because I did not understand what you meant above.

This would imply that natural selection is inadequate for explaining humans.

If A is impossible when B is true, then if you observe A, you can indeed conclude that B is false. I would happily agree with this logic. It remains to define what A and B are.

Thank you for your response. I edited the question to give an example of how "perfection" could be proved. Is it better now? Obviously, not being a biologist or even a scientist, I don't think I can give a precise experimental setup, but I don't see why the example I gave is not feasible. I have indeed read articles about "mathematics of consciousness" being at least a possibility within science. Edit: Also, I removed my claim that it would be the "only way" of disproving evolution, as well as "Darwinian".

@Raghib See my edit in response to your edit!

Even if all conditions required for point 4 were met, this would not disprove evolution (which could still apply to animals... or even mathematical functions themselves ...)

I basically argued that the only way it could be disproved was if one could prove that humans are somehow "perfect" (see below for definition) and for which the probability of evolving by natural selection was 0. This would mean that evolution could not explain the existence of humans in nature, and so natural selection would be disproved. While this is philosophical, the reason I posted it on here is because I am not a biologist, and am rather interested in what biologists would make of this idea, and whether it is just complete nonsense (which, not being a biologist, I do not deny)... My definition of "perfect" was that it would have to be mathematically proved perfection.

What you seem to be doing is asking us if a hypothetical, objective measurement of perfection was discovered and applied to humans, and whether or not Evolution would be "disproved" (obsolete as a Theory) by proving humans to be perfect.
If that's your premise; then no, proving human beings to be perfect does not disprove Evolution. Evolution is a process, a mechanism by which nature operates. That a perfect example exists of a thing does not invalidate the process by which it was made.

I also mentioned that the probability of this occuring naturally would be shown to be 0. I do not see how natural selection could still be true in that case, since it would clearly show that natural selection was inadequate for explaining humans.

@Raghib - So your suggestion appears to be that if humans were proven to be supernatural (or unnaturally perfect), then Evolution wouldn't apply to humans. Sure, that works -- but that's because scientific theories only apply to the natural world. Philosophically speaking, you're wrong because you're asking if the rules from Group A would apply to Group B when B is Mutually Exclusive from A. Or, for an analogy, you're asking if you can pitch a perfect game in football... It just doesn't make any sense.


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How do insects know what is edible?
What is the current scientific consensus on how insects innately know what is food and not food? If they are introduced to new food sources do they experiment with eating the new food? Could you teach a preying mantis to eat beef?

I think these are too many questions in one.

Insect feeding behaviour is generally triggered by one or more conditions which may include colour, shape, chemical traces or temperature.
Insects generally locate food based on some combination of olfactory, thermal and visual queues (colour and shape). If their minimum criteria are met to specified tolerance, they will attempt to feed on whatever is nearby using their usual feeding method.
When these conditions appear on the 'wrong' target, it attracts insects and triggers feeding attempts. Insects can be triggered to feed on atypical food sources if the relevant aspects of their environment match those of their normal feeding environments. For example, here is a report from a professor of entomology recollecting his observations of being bitten by pea aphids while handling plants, which he assumes is because of the scent on his hands.
We can exploit this in various ways for research. One is for artificial blood-feeding of insects: most systems, like the Hemotek membrane feeding system, warm blood to the body temperature of the host. They do not normally resemble a target host in any other way. Some blood-feeding insects have very specific requirements for temperature (for example they will only feed on blood if it is heated to the body temperature of birds; the same blood heated to mammalian body temperature will be ignored) but we do not need to make the target look or smell like the natural host. Other species may need olfactory cues, which can be provided by researchers rubbing the membranes on their forearms before placing them on the feeding system, or by breathing on cages as you add the food.
A second way we exploit this is for insect traps. Although not all traps work this way, some work by mimicking the host and attracting insects that are looking for a meal. This can be via olfactory/chemical mimicry (for example carbon dioxide baited traps - try Googling "CO2-baited traps") or visual. Different degrees of visual 'deception' may be needed; for instance to attract tsetse flies, colour is important but shape is not:

[tsetse traps] often use electric blue cloth, since this color attracts the
  flies. Early traps mimicked the form of cattle but this seems
  unnecessary

(https://en.wikipedia.org/wiki/Tsetse_fly#Trapping)
The exact reason why blue is so attractive to tsetse is unclear:

But, why are tsetse flies attracted to blue and black colors? What is
  the evolutionary advantage for them? It has been hypothesized that
  certain areas on humans, where tsetse like to bite, are a darker
  shade. Or, that the dark color simply identifies the object as not
  plants.

(https://www.acsh.org/news/2016/11/28/do-dark-colors-really-attract-tsetse-flies-10471)
If such behaviour increases the fitness of the insects, there is a selective pressure to change the cues used to identify situations where feeding behaviour is appropriate, which may result in consistent feeding shifts. We can infer by comparing insect taxonomy and feeding modes when shifts in diet have occurred. For instance, the moth family Calpinae has evolved piercing mouthparts to feed on fruit, but species in the genus Calyptra ('vampire moths') have adapted to feed on blood (which generally moths cannot access because their mouthparts cannot pierce the skin).

Maybe some interesting reading here:
https://www.ncbi.nlm.nih.gov/pubmed/27210550
"dopaminergic neurons (DANs) play a critical role in reinforcement and motivation"
"Olfactory learning in Drosophila could provide an inroad. Flies assign negative and positive values to odors in aversive and reward based paradigms"
Also
https://www.ncbi.nlm.nih.gov/pubmed/28334410


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If all animals were to die, would all plants die too?
Humans and many other animals are able to breathe because plants produce more oxygen than they need. I was thinking if all animals died all of a sudden, then wouldn't plants die too. Eventually they would produce too much oxygen and wouldn't have enough carbon dioxide to go through photosynthesis.

Animals are not the only organisms to respire without photosynthesizing. Fungi, many other eukaryotes and many bacteria respire too (and do not photosynthesize).
Now, if all animals were to suddenly die, there would sure cause a drastic environmental change for plants. Whether or not that would lead all plants to extinction is untestable and it is therefore impossible to give a definite answer. This type of question would be better suited for worldbuilding.SE. I personally doubt all plants would disappear.

Is this an attempt at an answer, a migration vote or a personal opinion? Your answers are usually of much higher standard Remi.b! ;-)


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Are there comprehensive species descriptions on most species?
I was having a browse through Wikipedia and noticed how even the rarest, hardest to find species of bird have comprehensive articles and comprehensive descriptions, but other species like the 1400 Andrena species have next-to-no information.
I tried to do a search for resources on individual species of Andrena bees but found very little - at best a short description and the name of the entomologist who described it. Is there a place I could go to find comprehensive resources on these bees? If not, why are the available resources on these species much less comprehensive than those on other species?

To suggest a new species, someone must necessarily makes a rather thorough effort of description. A good solution to get some info could be to go to the original paper however, these papers can be very old and hard to find. Also, the standards at that time might be very different from today's. After all, K. Linnaeus managed to describe 13,000 species also maybe because the description were more simple than they are today (see this related post). Andrena hattorfiana was described by Fabricius in 1775 but I could not find the original paper.
Note that the english wikpedia article for A. hattorfiana is relatively decent.
The IUCN red list is also a good source (see here)
The page for the Encyclopedia Of Life is unfortunately a little empty.
Here are some amazing pictures on flickr
You can also just search papers that refer to a given species. Here are a number of papers on A. hattorfiana.

Most species (at least 80%), by virtually all estimates, remain undescribed. However, we have described the most visible and obvious species.


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Pressure on the heart
Is there more pressure on the heart when lying down flat as opposed to lying down with head and knees slightly elevated?
Also is there more pressure on the heart standing up as opposed to lying down in either a flat or with head and knees slightly elevated


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Why DMSO is used as a control?
Coming from a non-biology background, I've realised many academic papers on experiments use DMSO as like a control. This is an example:

KN-93, a specific inhibitor of CaMKII inhibits human hepatic stellate cell proliferation in vitro

What make DMSO so special that so many scientists use it for their experiment and report their results? Why do we need it in the first place?

Its likely used as a control when its also being used as a solvent, not everything can be done in water

@zacdav Make your comment an answer, because that's the answer to the question.

Note that this is often described as a vehicle control. Essentially you are controlling for the effect of the solvent (ie the vehicle) used to introduce the compound of interest.

DMSO can be used as a solvent for a range of experiments. In these cases it makes sense to use the solvent as the control.


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Why roots have radial vascular bundles while stems have conjoint?
Why not the whole plant has the same arrangement of vascular bundle,  why there is a difference of arrangement in roots and stems (radial in root and conjoint in stem) ,  what is the purpose of this difference?


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Why do I have two kinds of pubic hair?
I feel silly even asking this question, but there's a quirk of my anatomy that I find interesting, and I can find nothing about it online.  I am looking for information on whether this quirk is documented, and whether it has any biological role.
I am a Caucasian male, and my quirk is that I have two different kinds of pubic hair.  On my genitals and immediately above, I have a dark wiry kind of hair like that which I find under my armpits and on my chest.  Above this, there is a second bundle of hair which is fairer (similar color to the hair on my head) and curlier.  The color difference between the two hair types is marked.  There is also a small amount of hair continuing up to my navel, which appears to be of the first type (same as chest, armpits, and genitals).
So my questions are:

Is this a common feature?
If not, is it documented at all?
Does it serve a biological purpose?

My reason for asking 3, in particular, is that I've heard multiple explanations for the existence of pubic hair.  One theory is that it indicates sexual maturity.  Another is that it is related to hygiene.  My anatomy seems to suggest both might be true: Hair under armpits is presumably for some practical purpose, like wicking sweat out of an otherwise dank crevice, and the hair on the genitals would appear to have the same effect.  On the contrary, colored hair like that on the head is presumably a secondary sexual characteristic, and the fact that I have a bunch of colored pubic hair above my genitals (where there is no apparent practical purpose, as with the hair below) would seem to serve the same purpose.

Relatively interesting evolution question --- hypothesis regarding reasons for certain evolutionary traits can be debated (this particular question, scientists seem to have many theories). However, here is one possible explanation:

Pubic hair near the sexual organs is likely for hygiene function; especially for women infections from parasites were common in those areas. The hair would act as a protection barrier, and hence the different texture of that hair being a little thicker.
Pubic hair in arm pit regions may keep pheromones, or chemicals your body produces that send subconscious messages to other humans. Often, these chemicals are released from sweat, and hence it would make sense to have hair in those regions to trap them there. The texture of the hair in those regions probably evolved to be more effective in keeping oder.

https://www.self.com/story/why-you-have-pubic-hair
https://blogs.scientificamerican.com/bering-in-mind/a-bushel-of-facts-about-the-uniqueness-of-human-pubic-hair/

what you are describing the the difference between terminal hair the coarsed darker hair an vellus hair the fine hair. Yes all adults have both.
 Vellus hair covers basically your entire body, Terminal hair mostly develops during puberty as a secondary sexual characteristic and only covers certain areas. the function of terminal hair and pubic hair is hotly debated and may differ from area to area. Proposed functions include friction/chafing prevention (armpits), scent retention, or even just as a maturity signal.


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Is there a organ or type of cell that makes Nagalase?
Schindler disease / Kanzaki disease is being described as alpha-N-acetylgalactosaminidase deficiency. So then, which organ or cell(s) produce this alpha-N-acetylgalactosaminidase (Nagalase) ?


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Is there any example, where cooperative behaviour of predators induce fear in prey population?
I am basically from math background and doing Ph.D in mathematical biology. So I am not so efficient in biology. But my problem based on cooperative behaviour of animals during hunting which is related to the animal behaviours in ecology.
We know that different animals show cooperative behaviour during hunting (or, group hunting) such as wild dogs, lions, chimpanzees, birds, spiders, crocodiles etc.
We also know that fear of  predator (predation risk) reduces the  growth rate of prey population. Now, I am looking for
example(s), in which prey population does not fear predator but cooperative behaviour of predators induces (creates) fear in prey.

Are you asking for exemples when a particular prey species is "normally" not afraid of predators, unless/until the predators displays a (cooperative) behaviour to induce fear?

@fileunderwater  Yes, you got my point. Could you please give me any example related to this phenomenon?

So an animals that is to big for one predator, but is hunted by a group of predators would suit your case? Then a giraffe hunted by lions comes to my mind. A lion alone wouldn't attack a giraffe, but a pack does. And they induce fear because they are many and show huntig behaviour.

Are you asking a question about prey psychology or prey behavior?  i.e. is it "fearful" behavior that is your focus?

Maybe relevant, in relation to fear: https://biology.stackexchange.com/questions/42497/are-there-any-animals-that-gradually-approaches-the-predator-to-search-for-food/42499#42499


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Hybrid, Japanese or European larch please?

pictured in NE Scotland 29th April

To tell these larches apart from each other the shape of the scales on the cones is a good place to start.
European larch have cones with scales that are straight, rather than curving outwards.
Japanese larch have cones with scales that curve markedly outwards as in this photo below.

From Wikipedia - Larix kaempferi
Hybrid larches, being a cross between the European and the Japanese, have cones that are in between. But as this Forestry Commissions publication,
 "Know your conifers", mentions there is some variation so it is useful to look at cones from more than one tree across a stand.
Summary: Your photo shows a cone with slightly curved scales or bracts, so I don't think that it is European larch. But it could be, it is slightly misleading as the seeds (the thinner bits are protruding).
Japanese larch cones are really curved, which when I was being taught tree ID were described as 'like roses'. So a definite, not Japanese.
So in my opinion it is most likely to be a Hybrid larch, but as the cone is not fully mature and open, and there is only one to look at it could be a European larch.
When looking at cones, I find it best to find old cones on the woodland floor that way you can see them at there most fully developed, and the differences between the species are more marked.
There is another ID feature between European and Japanese, and that is the colour of the stems. The former are straw-coloured and the latter are darker, brown/purplish colour. This becomes more obvious as the season progresses.
There are quite a lot of photos of cones on the web that have been given the wrong names, which makes it quite confusing. Best stick to Forestry Commission literature, or educational institutions.
When looking for photos I came across this YouTube video by Harper Adams University which is good and actually features the Japanese Larch photo that I found on Wikipedia.

Many thanks for your comprehensive and hugely helpful reply.  I will certainly look out for other clues as this is a single specimen growing in a small amenity stand of mature beech so it should be easy enough to monitor