text:
Meaning of "stripped" in "stripped antibody-depleted sera"
From a research paper:

FOLR1 autoantibody detection
The assay for identification of the presence and relative quantification of FOLR1 autoantibodies in serum samples was performed as previously published.41–43 Horseradish peroxidase (HRP) labelled anti IgG antibody (Cat#I8640 Sigma Aldrich) and IgM antibody (Cat#I8260, Sigma Aldrich) were used to detect IgG and IgM. Antibody-depleted sera (Sigma Aldrich) was used as negative control. Serum effect on blocking FA binding to folate binding protein was detected using HRP labelled FA (FA-HRP, Ortho-Clinical Diagnostics, Raritan, New Jersey, USA). FA in serum samples was removed as previously described. Unlabelled FA was spiked (0.01–2000 ng/mL) into stripped antibody depleted sera to generate the standard curve. The SuperSignal ELISA Femto Substrate (Cat#37074, ThermoFisher Scientific) was used as substrate for detection of HRP activity. Images were collected using a 96-well imager (Q-View Imager, Quansys Biosciences). Intensities were extracted from the images using Q-View Software. IgG, IgM and relative FA-blocking amount were calculated based on the standard curves.

What is the meaning of "stripped" in stripped antibody depleted sera? I think that "antibody-depleted sera" stands for "serum samples that contain a reduced concentration of antibodies". But why stripped? Does it mean that the authors applied some additional techniques to ensure an even lower level of antibodies in the serum samples?
I found it odd because the word "stripped" is used only in this particular place, and nowhere else. They mention 'antibody-depleted sera" earlier, without "stripped".

I think the word "stripped" refers to the depletion of FA (folic acid?). The previous sentence is "FA in serum samples was removed as previously described." They were probably clarifying that the standard was made using antibody-depleted, FA-depleted (stripped) serum.

@MattDMo - thank you! Indeed, in a paper referenced in "as previously described", a charcoal stripping method for removal of folic acid is described. You might post your comment as an answer, it was the correct guess!

All set - I posted an answer below.

While @mgkrebbs is correct in their answer that the meaning of "stripped" cannot be 100% determined without corresponding with the author, there are clues that point to  a most likely answer.
The previous sentence, "FA in serum samples was removed as previously described", cites this reference, which describes testing of different materials for their efficacy in removing radiolabeled folic acid from serum. I don't have access to the full text of that article, but according to the original poster of this question, this method was called "charcoal stripping."
The term "stripped" is also commonly understood in the lab as referring to some reagent which has had some component(s) of its makeup removed intentionally. The two uses I'm familiar with are this scenario, where some component of serum is removed (usually with charcoal), and western blotting, where stripping refers to the process of removing the bound antibodies from the membrane so that it can be reprobed with different ones.
So, with no other depletion method being mentioned aside from the antibody depleted serum purchased from Sigma, the arrangement of sentences, and the reference to charcoal stripping, I think it's safe to assume that "stripped antibody depleted sera" refers to the Sigma reagent which has undergone the folic acid removal process.

I believe this is a failure of editing, and the meaning in this paper of "stripped" cannot be determined without correspondence with an author.  "Stripped" is an informal term for either removal of some substance or treatment with a material such as charcoal which affects many substances. Normally in papers "stripped" is qualified (at least initially) to indicate the type of treatment.  Here it could plausibly refer to antibodies, folic acid, or any number of other things.  It may be an artifact of draft editing that was meant to replace "stripped" with "antibody depleted" as a more precise term.  I suggest writing the corresponding author.


text:
meaning of "usually greater than 200 base pairs"
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

Homologous recombination. All cellular organisms have molecular functions dedicated to recognizing and recombining DNA molecules that have extensive sequence similarity at the region of cross-over, usually greater than 200 base pairs. The principle molecule involved in homologous recombination belongs to the family of RecA/Rad51 DNA binding enzymes that catalyse post-replicative strand exchange during meiotic/mitotic recombination or repair of DNA double-strand breaks. These enzymes show some sequence preferences (Raja et al., 2006) and require minimally efficient processing segments of 20–30 base pairs to initiate strand exchange (Majewski and Cohan, 1999).

I'm not sure of the meaning of "greater than 200 base pairs". Does that relate to "sequence similarity"? Is similarity somehow measured in base pairs?
Or does that relate to "the region of cross-over"? Is the meaning "the region of cross-over is usually greater than 200 base pairs"?

No, similarity is not measured in base pairs. They are talking of regions of cross-over being marked by at least 200bp of highly similar sequence between the two strands involved in exchange.

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text:
What is the meaning of "leukemic cell recovery" in an abstract?
An article abstract:

Significant predictors of treatment outcome are poorly defined for patients with T-lineage acute lymphoblastic leukemia (T-ALL). A high WBC at diagnosis, which has traditionally been a predictor of poor response in T-ALL, has considerably weakened prognostic significance in the face of modern, more intensive chemotherapy. To test the hypothesis that bone marrow stroma-supported leukemic cell recovery might identify children at high risk for relapse, we measured the ex vivo recovery of T-ALL lymphoblasts from 29 newly diagnosed patients using a stromal cell co-culture assay. In all cases the T-ALL lymphoblasts showed an increase in recovery of T-ALL cells (RTC), ranging from 4 to 343%, in comparison to samples maintained without stroma. Since we were blinded to patient outcome in this case-control study, we then correlated patient outcome with RTC. The RTC for 18 patients in complete continuous remission (CCR) for greater than 4 years was stochastically larger than for the 11 patients who eventually relapsed (P = 0.011, by the two-sided Wilcoxon test). Furthermore, 100% of patients with an RTC of more than 26% had a CCR greater than 4 years while 78% of the patients with an RTC of less than 25% relapsed within 4 years. This is the first report to show that higher lymphoblast recovery may predict a more favorable outcome for children with T-ALL. A prospective study is needed to test whether stroma-supported leukemic cell recovery might serve as a basis for assigning risk-adjusted therapy.

What is the meaning of recovery here? It puzzles me as a non-native speaker of English. Do the authors simply mean "the number of cells that survive"? Or is there some "recovery process" - if yes, what is the nature of this process?
P.S. The question arose from a question asked by a fellow translator. She translates a text in which T cells transduced with gene for a receptor against leukemic cells are co-cultured with such cells, after which

"T cells transduced with the receptor markedly reduced leukemic cell recovery".

The translator has trouble understanding how to put it in Russian, because translating "recovery" verbatim would imply some process in which a cell recovers, say, from injury.
Is "recovery" just "the percentage of cells that survived, relative to the overall number of cells"?

I don't think this is a great place to ask, unless a bona fide hematologist answers, and who can assure that? The term is confusing. In your place, I would check with a hematologist. It's not a common term.

TL;DR: Yes, it's just percentage of cells that survived. With the caveat that the assay doesn't give information on how much the number of cells is influenced by survival, dying, or growth rate.
"Recovery" in this context means "cells found after X amount of culture time". Generally speaking, recovery often refers to putting something in a program/dish/liquid/organism and seeing how much is still left after some processing/treatment/culture. For example, if I give a 1-year-old child 10 porcellain plates to play with, I might be interested in what percentage I can recover after 2h of play time. Of course in the context of cell culture, that percentage can be above 100% if the cells multiplied in the meantime.
As the methods of the article describe, the culture assay consists of first growing a single layer of stromal cells (HS-5 cells) on a culture plate for 24h. These cells provide support for the actual cells of interest. The researchers then spread 5.0 × 105 viable T-ALL lymphoblasts isolated from a patient sample on the stromal cell layer. They do this twice* for each sample, in one case collecting the cells after 1h (which isn't usually enough time for human cells to do anything), in the other case collecting them after 72h of culture (which is enough for healthy cells to grow substantially). Then they use flow cytometry to quantify how many T-ALL cells are now in the culture after that time has elapsed.
This helpful graphic is from the paper. The word "cells" in the formula refers to T-ALL cells.

The percentage of recovered T-ALL cells (RTC) was calculated by:

Essentially, what the authors here studied is whether the likelihood of a T-ALL patient to relapse might be related to the ability of their cancerous cells to survive or grow in a culture dish coated with stromal cells.
The quote from your colleague would mean that the T cells were surviving/growing less or dying more if they were transduced with the receptor.
*rather, four times. Twice for 1h and twice for 72h collection. At least this is what "in duplicate" implies.

Why do the authors use ex vivo instead of in vitro for their culture? I found the term ambiguous, and only used 13 times (can't remember exactly) on Googling with Scholar. But nice answer.

In my understanding, ex vivo is a subclass of in vitro, although it's not something I would associate with primary culture of lymphoblasts...

Thanks. My understanding of ex vivo is, say, bone marrow. But if it's cultured, it's not ex vivo (it's been grown.) Anyway, I didn't have full access, but thought the paper was not without ambiguities. Again, thanks. (btw, the term I found ambiguous was leukemic cell recovery). For a cancer so well studied, to find it so few times was interesting.

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Does Goryaev's chamber have the same grid layout as the conventional counting chamber used in the West?
I'm translating a Russian biotec text where some cell counting operations are mentioned. The piece of equipment the authors mention in this context is "Goryaev's chamber" (камера Горяева):

We discarded the supernatant, washed the cells with DPBS twice (suspended and centrifuged them for 10 min at 200 g), then diluted with 10 ml of ADCC assay medium and assessed the concentration and viability of the cells in a Goryaev's chamber.

Is a Goryaev's chamber any different in terms of its counting grid layout from the conventional hemocytometer chamber described in Wikipedia?
I would like to translate the phrase simply as "using a cell counting chamber" or "using a hemocytometer". The Multitran dictionary does offer these words as possible translations, but it occurred to me that Goryaev's chamber might differ somewhat.

From the description at http://cldtest.ru/hdbk/chamber
It appears to be functionally the same device, except the only the smallest square are marked (0.25 nL and 4 nL), and the total capacity is 90 nL instead of 100 nL. A hemocytometer could be used in place of a Goryaev's chamber (though not necessarily the reverse).

Welcome to the site, Eliane!


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Meaning of "optical" in "Optical cap, 8X Strip" (used in qPCR)
I'm translating an English document that lists equipment used in a qPCR procedure:

Reagents/Materials

Optical cap, 8X Strip

I googled and found that the meaning of this line is "a strip of 8 caps for PCR tubes". What is the meaning of optical though? I'm not sure how to translate it into Russian.
Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?
Screenshot:

I'm googling but I can't seem to find any definition of "optical cap". It is used in a lot of books and documents as if the term is self-evident, while it's not.

I think it means flat-top, please refer to the article.https://www.thermofisher.com/order/catalog/product/4323032#/4323032

Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?

Yes and yes. As an example of the different kinds of PCR tube caps, refer to the cap options available from Thomas Scientific:

Available with a domed, flat frosted, or flat clear caps for qPCR. [emphasis mine]

For most lab plastics, "optical" refers to the surface between the camera/detector and the sample.  Another example: for plate-based fluorescence assays where the plate reader takes measurements from below  the plate, one might use a Nunc MicroWell 96-Well Optical-Bottom Plate from ThermoFisher. Usually, such plates also have opaque walls to prevent signal bleed from adjacent wells.

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How do I name a binding antibody? “Binding antibody to”, “binding antibody against”, or “anti-[antigen] binding antibody”?
I'm translating a text that describes how an immunogenicity of a drug is measured by assaying the levels of binding antibodies to the drug. Or is it "against the drug"? I'm wondering how to name these antibodies. Let's say the drug is cetuximab, and I'm writing the title of a document section:

Assay of binding antibodies against cetuximab in serum.
Assay of binding antibodies to cetuximab in serum.
Assay of anti-cetuximab binding antibodies in serum.

I googled for "binding antibodies to" and "binding antibodies against" and got only several dozen results for each of the two options. Therefore I came up with "anti-[name of the antigen] binding antibodies", but don't know how to google for it, hence my question here. Would option 3 look nice to a native speaker?
P.S. Alas, it is exactly "binding antibodies to" in my Russian text. I cannot omit the adjective "binding" before "antibodies"..

Связывающие антитела к цетуксимабу.

I quote from the Wikipedia page on neutralizing antibodies:

Most antibodies work by binding to an antigen, signaling to a white blood cell that this antigen has been targeted, after which the antigen is processed and consequently destroyed. The difference between neutralizing antibodies and binding antibodies is that neutralizing antibodies neutralize the biological effects of the antigen, while binding antibodies flag antigens.

My authors use the adjective "binding" to distinguish binding antibodies from neutralizing antibodies, just like in this paper, for instance: BAbs and NAbs. Another section in my document gives the results of an assay of NAbs against the same antigen.
Explanation of the difference between binding and neutralizing antibodies from the FDA:

(ADA: anti-drug antibodies)

Not worth an answer, just a comment: antibodies can be abbreviated to Ig, too, so in-text you could also call them "anti-cetuximab Igs" if you find the full expression to be too verbose.

@xusr - I'm afraid "assay for" would imply only the description of the procedure, but in my case the section describes both the procedure of antibody concentration measurement and the results of the procedure. Would of look really odd there?

The adjective “binding” is not used to qualify “antibody” in English scientific usage because linguistically it is thought to belong with the antigen the antibody binds.
Generally it is omitted if the prefix “anti” is used, e.g.

anti-cetuximab antibody

(e.g. “two or more anti-hapten antibodies” here)
However if you wish to refer to the particular small portion of the antigen that is recognized (the epitope), you might write, e.g.

tyrosine-binding antibody

(e.g. “Hapten‐binding antibodies…” here)
As far as the use of prepositions is concerned, “to” is used with binding, although it is optional. However generally with the antigen, e g.

cetuximab binds to the antibody

(e.g. “Antigen binds to the antibody on the B-cell membrane.” here)
But

the antibody binds cetuximab

(e.g. “An additional VNAR, Help6, which binds Hepatitis B precore protein” here.)
Completely illogical, I know, and this distinction is not universal.
However, “against” is used in relation to preparing or raising antibodies, e.g.

We raised an antibody against cetuximab…

(See the legend to Fig 1. in this paper.)
So in general one would write:

Assay of anti-cetuximab antibodies in serum

Addendum: Binding antibodies v. Neutralizing antibodies
The revised question makes it clear that the authors are referring to “binding antibodies” as a specific contrast to “neutralizing antibodies”. This expression was not known to me (I am not an immunologist), and, although the poster documents it, its use would appear to be limited, perhaps because the topic is or was controversial.
The question remains, how to express this idea in a clear and unambiguous manner, with the specific problem that the poster is a translator, not an editor. I would still try to avoid the use of the word “binding” in the expression. I have two suggestions:

I believe that an alternative expression would be “non-neutralizing antibody” (the paper just quoted does not hyphenate this term, but others do, and I would). If this belief is correct, one could write:

Assay of non-neutralizing anti-cetuximab antibodies in serum

Alternatively one could use the abbreviation, “BAb”, from the paper cited by the poster, although this would have to be defined somewhere.

Assay of anti-cetuximab BAbs in serum

Indeed, you are correct, good sir. You know what they say - there's more than one way to refer to an antibody!

I was preparing this answer on SE EL&U when some idiot commented that he should post elsewhere — not necessary — and I couldn't post my answer as the question had been deleted. Hence the somewhat linguistic tone.

Ah, but the linguistic tone is not at all out of place in SE Biology; quite the contrary, it is most welcome.

@Stefan — Not what I was saying earlier today, but I could hardly send him back to EL&U.

I know. I mean I enjoy the linguistic tone no matter where I come across it.

I figured it out. My authors use the adjective "binding" to distinguish binding antibodies from neutralizing antibodies, just like in this paper: BAbs and NAbs. Another section in my document is dedicated to the results of an assay of NAbs against the same antigen.

I have included an addendum in response to your clarification. As both Stefan and I were confused by the use of the word “binding” I would still advise against using it.

@David - thank you for the addendum, David! My customer won't ever let me edit out the adjective "binding".. Because there are many translators working on many documents for this customer, and the majority of them will use the word "binding" as an adjective there without blinking an eye, and it would be sheer hell to make them all adhere to "non-neutralizing" or to just "BAbs". But thank you for your effort!

@CopperKettle — Sure, I understand your situation. I'd go for 3, then, perhaps hyphenating binding and antibody to emphasize their association.

In English, you say that antibodies bind to something (X), not against something. You can use the phrases "X-binding antibodies," "X-specific antibodies," "X binders" (when referring to the antibodies that you've previously introduced in the text), to name a few. You can use "antibodies binding to X," but not "binding antibodies to X," people will misinterpret the latter, because it means something else is binding to the antibodies or you are trying to bind something to the antibodies.


text:
Land recultivation? Land revegetation? Land reclamation? Land rehabilitation?
I'm translating a Russian text about the recultivation (рекультивация) of land formerly used for open-pit mining. The process of 'land recultivation' in Russia involves three general stages:

Preparatory stage: a feasibility study, justification of investment, development of working documentation.
Technological stage: engineering operations that involve large-scale movement of soil, removal of machinery and buildings, etc.
Biological stage: seeding of trees and plants, soil improvement operations, irrigation & drainage work, etc.

It is said that the last two stages can last for "years or even decades".
Which English word should I pick? Recultivation, revegetation, reclamation, or rehabilitation?
Example sentences (I retained the original "recultivation" here):

All too often a coal mining company implementing a recultivation project in this region limits itself to the use of simplified technological solutions that fail to take into account the need to preserve biodiversity. The range of plants used at the biological stage of recultivation is limited to five tree species, which depletes the genetic resources of the region's ecosystems and exacerbates the existing invasive species problem.

P.S. The authors of the text do no imply that the land should be used for agriculture - to the contrary, their goal is to improve biodiversity.
P.P.S. Here is a newspaper article about this "recultivation" of open-pit mine land in Kuzbass: source (in Russian)
P.P.P.S. I've just discovered that the English-language title of the Russian national standard GOST R 57446-2017 that comes into force on 1 December 2017 translates the term as land reclamation. However, those who translate Russian documents into English are not always correct.

I think the word choice depends on the ultimate intended use of the land, e.g. recultivation would be appropriate only if it's intended to grow crops.

@jamesqf - growing crops is out of the question - their goal is biodiversity restoration. Maybe I should pick revegetation then.

I'd say that rehabilitation would be the best choice for intending to improve biodiversity.  Simple revegetation would be what's done by the coal companies in that quote.  I think reclamation would be a generic term that includes all the others.  But I'm commenting as just an ordinary English speaker, not a professional in the field.

@jamesqf reclamation is the term I see most often in English texts about this subject. However, I'm no native speaker, so can't really judge it.

Reclamation can be used in this context, but I think in this situation the most appropriate word would be "remediation", from the Latin word remediare which means "heal" or "cure". It is most often used in the sense of fixing environmental problems such as pollution or contaminants.
https://en.wikipedia.org/wiki/Environmental_remediation
A Google search suggests this is a widely used term in the mining industry for the situation you describe.
https://www.google.co.uk/search?q=remediation+mining
It does depend exactly which stages you're attempting to describe, though. From http://www.miningfacts.org/environment/what-happens-to-mine-sites-after-a-mine-is-closed/:

The terms reclamation, remediation, rehabilitation, and restoration
  are all used to describe mine closure activities that attempt to alter
  the biological and physical state of a site. [11] The terms are
  sometimes used interchangeably, and are closely linked, but refer to
  distinct steps in the preparation of the site for another use: [11,
  12]
Remediation: The cleanup of the contaminated area to safe levels by removing or isolating contaminants. At mine sites, remediation
  often consists of isolating contaminated material in pre-existing
  tailings storage facilities, capping tailings and waste rock piles
  with clean topsoil, and collecting and treating any contaminated mine
  water if necessary.
Reclamation: The physical stabilization of the terrain (dams, waste rock piles), landscaping, restoring topsoil, and the return of
  the land to a useful purpose.
Restoration: The process of rebuilding the ecosystem that existed at the mine site (where applicable) before it was disturbed. The
  science of mine reclamation has evolved from simple revegetation
  activities to a discipline which involves using native plants to mimic
  natural ecosystem development over an extended period of time. [13]
Rehabilitation: The establishment of a stable and self-sustaining ecosystem, but not necessarily the one that existed before mining
  began. In many cases, complete restoration may be impossible, but
  successful remediation, reclamation, and rehabilitation can result in
  the timely establishment of a functional ecosystem.

See also this publication by USGS:
Finger, Church, and Guerard. Potential for Successful Ecological Remediation, Restoration, and Monitoring, Integrated Investigations of Environmental Effects of Historical Mining in the Animas River Watershed, San Juan County, Colorado, 2008; U.S. Geological Survey Professional Paper .

Thank you! Based on the definitions you provided, I'd pick rehabilitation because the bulk of my document is concerned with restoring the steppe/meadow ecosystem at the spoil tip sites.

Can reclamation include rehabilitation? I'm getting tangled in all this.

Reclamation is about the physical geography of the site, rehabilitation is about the ecosystem (I think). I'm not sure if rehabilitation and bio-/phyto-remediation overlap though!

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text:
What exactly is "lateral septum"?
I came across the phrase lateral septum and I can't seem to find the precise definition online. Is it "the areas roughly to the right and the left of the septum pellucidum"? Or is it the parts of the septum pellucidium itsef? I'm confused.
If it is near the septum pellucidum (to the left and right), does it include particular nuclei?

Brain pathways for sexual excitation involve the activation of incertohypothalamic and mesolimbic DA transmission in the mPOA and NAcc that focuses attention on incentive sexual stimuli and engages motor patterns of approach and consummation. Collectively, the behavioral patterns stimulated by those systems and the subjective feelings that accompany them constitute the epiphenomenon referred to as sexual desire or, when mixed with genital and sympathetic arousal, “libido.” The core of this pathway includes the mPOA and its outputs to the VTA, which contain DA cell bodies that project to various limbic and cortical regions, such as the prefrontal cortex, olfactory tubercle, NAcc, ACC, lateral septum, and corticomedial amygdala.

The article is "Pathways of Sexual Desire" by James Pfaus (2009).
I have read the Septal area article in Wikipedia but still cannot get it.

It is confusing.  The septum pellucidium is a thin membrane separating the left and right lateral ventricles.  It contains white matter (nerve fibers), blood vessels and a few neurons.  It has traditionally been thought of as just a separating membrane, but the fibers running through it connect to the hippocampus and hypothalamus and so it is probably a relay to those structures.
Lateral to the septum pellucidium are the septal nuclei. The septal nuclei are NOT considered part of the septum pellucidium (or vice versa).  The septal nuclei are traditionally divided into two major subregions, the medial and lateral septal nuclei.  As you might have guessed, the medial nuclei are immediately adjacent to the septum pellucidium.   As the septum pellucidium is quite thin, the right and left medial nuclei appear to compose a single midline nucleus with the septum pellucidium running through it. The lateral nuclei are the ones a bit further out and it is these that are called the lateral septum. The septal nuclei may be further divided into caudal and ventral regions.  Many neuroanatomists group the most posterior parts of the septal nuclei into a third group, the posterior septal nuclei distinct from the lateral and medial divisions.
This is part of the problem.  Structures in the brain were named based of where they were and what they looked like since their functions were unknown. For example the hippocampus was given this name because it looked like the tail of a seahorse (genus Hippocampus), and the locus ceruleus ('blue place') looks blue. As we have learned more, some neuroanatomists have divided regions into subregions or sometimes lumped regions together based on their models of the proposed physiologic functions or neurochemistry of those regions. The subcortical 'limbic' nuclei, including the septal nuclei are among those most subject to these changing definitions,.  And as you might guess, different neuroscientists often disagree about these divisions.  Being human, they sometimes behave as though their definitions are THE definitions, or gloss over differences between sometimes unclear definitions.  Ideally, people splitting nuclei into proposed subregions try to propose clear definitions, but this is not always the case and these proposed definitions may not be accepted or used.  This can make it difficult for experts to know exactly what regions are being discussed, let alone people not long immersed in the field.  Over time however, fields tend to come to a consensus on terminology though for many brain regions this consensus remains elusive.  I hope this discussion makes the topic of the lateral septum a little more comprehensible, if only by validating your sense that the topic is confusing.
Here is a readable overview about the septal nuclei and septum pellucidium:https://www.neuroscientificallychallenged.com/blog/know-your-brain-septum
Check out the first reference here to discussing the neurochemistry of the medial septal nuclei from a chapter by Risold in the Rat Nervous system https://www.sciencedirect.com/topics/neuroscience/medial-septal-nucleus
In contrast look at the introduction of the following paper regarding the lateral septal nuclei:
https://bio.biologists.org/content/8/7/bio043554
"Whole-brain mapping of projection from mouse lateral septal nucleus"
And if you have access, you may be interested in
https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.13746
"Differential and complementary roles of medial and lateral septum in the orchestration of limbic oscillations and signal integration"
And here is a paper that describes development of the posterior nuclei as being different from that of the lateral and medial nuclei
https://www.nature.com/articles/s41598-018-30020-9


text:
Difference between "wash" and "rinse" in biotechnological procedure descriptions
Is there a difference between "rinse" and "wash" in sentences like this:

Following the staining, the sections were washed twice with deionized water, then dehydrated using ethanol solutions of incrementally increasing concentration (70%, 80%, 96%), cleared using a xylene substitute, embedded in the mounting medium and coverslipped.

Can we use "rinsed" freely in the place of "wash" here, or are there nuances of meaning?
I know the difference between the two verbs in non-specialized English, but I'd like to know if there's a difference in a biotech procedure context.
Google Ngram search gives the following for "sections were washed, sections were rinsed":

I think they mean the same it is only the usage of different terms.

@Chris - thank you! Iooks like "wash" wins out.

My chemistry lab teacher told us the difference between rinsing and washing before explaining titration. According to what she told, rinse - just cleaning from the outside wash - thorough cleaning from outside as well as inside Another difference was that rinsing was done using water(only), whereas washing included cleaning with HCl also.

This is a very interesting question and it's kind of strange there doesn't seem to be any literature on it. One would expect those to have been carefully studied by the designers of automated microtechnique equipment such as tissue processors and slide stainers.
I own a fair amount of literature on microtechnique, ranging from the end of the 19th century up to the 1980's. I went trough some of those briefly this morning, but I couldn't find a definition for "dip", "rinse" or "wash" or their German, French, Dutch equivalents (And there are a lot more of those, such as "drain", "agitate", "flood", ...).
The problem is even more complicated than it looks alread, as, very often those terms are acompanied by an adjective adding even more confusion, such as "quick/slow dip", "brief rinse", "thorough wash" etc.
I suppose (but that's only speculation on my part) those therms being undefined has to do with the fact that, in microtechique there are that many variables involved, that it's often next to impossible to achieve reasonable results without esoteric stuff such as "technicians experience" coming into play. That's defenitly the case in the field of for example staining technique, when "the classics", such as Masson, Mallory/Heidenhain's AZAN, Van Gieson etc... need to be used.
But not only in that field: If you do some reading in mailing lists such as the Histonet Listserver, you'll notice that messages, questions etc. on "inadequate processing schedule", "reprocessing inadequatly paraffin infiltrated brain/heart/liver/pancreas/... tissue", "bubelled nuclei and an unidentified artefact", "Feulgen stain doesn't work!" are fairly common occurences. Regardless of how expensive the equipment, regardless of however wel reviewed the protocols, regardless of however strict the quality control.
The only -brief- definition of "dip", "rinse" and "wash" I know of and I can remember, is in the book I have, but I can't find for the moment (you'll always see it...):
Smith, A., Bruton, J.: "A colour Atlas of Histological Staining Technique",
? th edition, 1977, ISBN: 07234 0721 5
Publisher: Wolfe Medical Publications Ltd, UK.
Perhaps you'll get any further, starting from there.
O, and while probably pointing out the obvious: dip is shorter than rinse is shorter than wash.


text:
What is the difference between Endoproteinase Lys-C and Lysyl endopeptidase?
What is the difference between Endoproteinase Lys-C and Lysyl endopeptidase?
In the text I'm translating about peptide mapping, "lysine protease" is mentioned (in Russian: лизиновая протеаза). This might be erroneous to translate word for word as "lysine protease". There must be a slight error in the original text. This "lysine protease" is mentioned there due to its use in protein hydrolysis.
I guess that the correct translation might be either endoproteinase Lys-C or lysyl endopeptidase.
I found that endoproteinase Lys-C is used in peptide mapping. Is it synonymous and interchangeable with lysyl endopeptidase, or do they differ in their function? Is endoproteinase Lys-C used more often as a hydrolysis agent in peptide mapping?
Maybe the difference is that endoproteinase Lys-C cleaves "on the C-terminal side of lysine residues", while lysyl endopeptidase cleaves on both sides?


text:
What word/expression is used to describe a band's share in the stained portion of the electrophoretic lane?
I was translating the following sentence from Russian, and realized I was not sure how to put it right:

The study shows that the electropherograms of the studied samples of DRUG NAME obtained in reducing conditions contain two clearly delineated bands with a mean total coverage of 99%, while the minor bands have a coverage of 1%.

The intended meaning is: of the whole stained area of the lane, the two principal bands cover 99%, while the minor bands only contribute an insignificant amount: 1%.
The original Russian word is содержание (content), but this is ambiguous, because we are really describing the contribution of the bands.
I'm not sure what word/expression to use. Is this "coverage" traditionally measured as the area, or as the length, of the band relative to the total area/length of the lane? How is it usually described?

You can compare band thickness but if a band is occupying more than 5% of the lane (of a usual SDS-PAGE gel) then it is not really a good band and you need to reduce the protein amount in the sample. Moreover, these kind of band quantifications (of specific proteins) are usually done after western blot.

@WYSIWYG  - the bands really occupy only a minor part of the actual lane, it's that the two principal bands contain 99% of the staining, I mean, of the dyed part of the lane.

@WYSIWYG - the word might be density, according to this document. They measure density of the bands, then look how much this or that band controbuted to this total density.

You might also try posting to Math SE. A representation of data is essentially a mathematical object, and mathematicians tend to be very precise with their words. If you just want non-expert suggestions, I might say "accounting for 99% of the stained area".


text:
Is there a specific English term for this vessel for microbial sampling?
In Russian, such a container (see pictures) for microbial sampling is called бакпечатка (bakpechatka), as I learned just now. I've no idea about the etimology of the Russian term. Probably "bak" stands for "bacterial" and "pechat" is for "print" (to press).
This deep container is used for taking bacterial samples by pressing a part it against the patient's skin or mucous membrane and then putting the material that stuck to it into an agar medium. Probably the "pressed part" used for sampling is the white cup, and agar is inside the container. At least that's what I gathered from scarce descriptions online.
Are there similar containers for bacterial sampling in the West and what is their name?
Thus far, I'm calling them "bakpechatka culture cups" in the document I'm translating, in the hope that the English-language reader will google and look at the pictures online.

Apparently it is called Count FlexiPlate, although this might be a brand name of a product produced by HiTouch (just as Aspirine can be only the acetylsalicylic acid  produced by Bayer), see here. Note also that it is a modified version of Petri dish, so the latter name may apply as well.


text:
What is the "GTP activator protein" that activates GTP-cyclohydrolase-1?
From GTP-cyclohydrolase deficiency responsive to sapropterin and 5-HTP supplementation: relief of treatment-refractory depression and suicidal behaviour (BMJ Case Reports, 2011)

The metabolic profile reported here is unique to GTPCH deficiency or a defect in the GTP activator protein. While there is no known demonstrated defect in this protein, it would cause similar functional deficiency. Other enzymatic defects in the pterin synthetic pathway present with very different metabolic profiles.

I googled but could not find a particular "activator protein" that interacts with GTP cyclohydrolase I. Is this one of the GTPase-activating proteins? They must be numerous, and I haven't found one that was shown to activate GTP cyclohydrolase I.
At the same time, the authors use the definite article, as if this protein is known. I'm intrigued.
I found this paper, in which GTP cyclohydrolase I is said to interact with Rho-GTPase-activating protein 7 (also known as DLC1), but the paper does not say that this protein is an "activator", they merely list it as part of the putative transcriptome of GTP cyclohydrolase I.
Further, in the quote the authors say that "there is no known defect in this protein", but the OMIM page for DLC1 says that a defect was known from at least 2000, although it is related to cancer, not to the BH4 pathway.

Perhaps this protein?

@canadianer - thank you! It might be it!


text:
Is homocysteine converted to glutathione during oxidative stress?
From the paper titled "The basis for folinic acid treatment in neuro-psychiatric disorders" by Ramaekers et al., 2016:

On the left side of the figure, the purine metabolite GTP serves as the substrate for the GTP-cyclohydrolase I enzyme (GTPCH) to produce tetrahydrobiopterin (BH4), which is the co- factor for enzymes producing dopamine, serotonin and NO.
  At the upper right of the figure the trans-sulfuration pathway is shown.
  It converts accumulated homocysteine to the anti-oxidant glutathione during oxidative stress.

Is this so? Is it true that this pathway is only active when the cell is under oxidative stress conditions?
Or maybe the authors meant to say that the pathway converts homocysteine to glutathione, which is later used to counteract oxidative stress?
Here's the figure from the paper:

Is English your first language? The statement "It converts accumulated homocysteine to the anti-oxidant glutathione during oxidative stress" has no qualification such as "only" that would restrict the conversion to oxidative stress. It does not preclude that this is the general pathway for synthesis of glutathione for use in any situation where its reducing power is required. And you will find that almost certainly to be the case if you research the pathways of glutathione synthesis, e.g. here.

I'm voting to close this question as off-topic because it is based on a misunderstanding of a sentence in a paper and thus has no general value for SE Biology.


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Meaning of letter "c" in description of mutation: "Homozygous c.195C>G; (p.Cys65Trp)"
In a table in a paper titled Cerebral folate deficiency: Analytical tests and differential diagnosis, there's the following description of a mutation in a patient:

Homozygous c.195C>G; (p.Cys65Trp)

I wonder what the letter c means here.

Well, if it is not in the paper, I’d try emailing the authors. They should know.

@David - thank you! I just imagined this might me a super-easy question, that's why I asked here.

It’s not. There will be people in the field who will know, but it would be good if the authors were made aware of the narrowness of their writing (if this is, indeed, the case).

I typed "c dna mutation" in Google and this article was the first hit:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867422/
The "c" denotes coding DNA, which given the context of the amino acid mutation having the letter "p", this makes sense.

It means coding DNA reference sequence. Please refer the following link for more information. https://varnomen.hgvs.org/bg-material/simple/ . This should help.


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Meaning of "standard reactions" in a DNA extraction procedure description
From a DNA extraction procedure description (an in-house pharma document I'm translating into Russian):

Preparation of Standards

All the standard reactions should be prepared at least in duplicates. The template DNA stock (CHO cell genomic DNA) should not be less than 100 ng/μL concentration.

Does "standard reactions" here mean what it says, or does it really mean "reactions with standards" (reactions using standard samples)?
P.S. It is part of a qPCR procedure to quantify host cell DNA content. The company is producing a monoclonal antibody drug and is describing its internal procedures. As a translator I cannot disclose the document in full.

https://meta.stackexchange.com/questions/320052/why-are-images-of-text-code-and-mathematical-expressions-discouraged

How can we possibly know?

In order to quantify a target using real-time PCR, each run must include a standard curve of your target DNA. This is typically done by making serial dilutions of some known quantity of template DNA, with each dilution assayed in duplicate or triplicate on the same plate as your experimental samples of unknown quantity. A standard-curve is also important for determining assay validation statistics like amplification efficiency (reference).

Does "standard reactions" here mean what it says, or does it really mean "reactions with standards" (reactions using standard samples)?

Since your protocol is designed to quantify host DNA, I would interpret the phrase "standard reactions" as referring to the actual qPCR reactions containing standard dilutions, not necessarily to the DNA extraction procedure. The reason there is a specified minimum concentration for the standard template DNA is likley a quality control check to prevent errors caused by degradation of DNA standards during storage or from freeze-thaw activity. The quality of your qPCR data can only be as good as the quality of your standard curves.
Reference:

Real-time PCR Handbook, published by ThermoFisher Scientific (Lifetechnologies.com)


text:
Is "TATA signal" synonymous with "TATA box"?
In the text I'm translating I have a diagram of an expression vector. It has a lot of marks, and one says "TATA signal". I googled and found the expression "TATA box".
Are these expressions fully synonymous and interchangeable?
From Wikipedia:

Considered to be the core promoter sequence, it is the binding site of either general transcription factors or histones (the binding of a transcription factor blocks the binding of a histone and vice versa) and is involved in the process of transcription by RNA polymerase.

So basically "TATA box" serves as a signal to the transcription machinery that says "transcribe this"?

Is this TATA signal in the figure very close to the transcription start site?

@Chris - it is positioned just before the target gene (which we want to express) and just after the GAPDH promoter. I'm not sure where the transcription start site is on that diagram. Maybe the beginning of the target gene sequence is the transcription start site?

@Chris - but it's quite far from the origin of replication

The ori doesn't matter here - if it is located immediately upstream (around -25-35 if I remember correctly) then it should be the TATA box.

@Chris - if the ORI is located immediately upstream? Or if the TATA signal is located immediately upstream of the target gene?

I guess that you have a expression plasmid of some kind that you are looking at. There it doesn't matter, where the ori is. Only the position of the TATA box (or signal) relative to the TSS is important.

Probably this is the reason why they call it a TATA signal instead of a TATA box:

The TATA box was originally identified as a regulatory signal upstream
of many protein-coding genes transcribed by RNA polymerase II (Pol
II). However, some tRNA and 5S RNA genes and most RNA polymerase III
(Pol III)-transcribed genes with external promoters also possess TATA
boxes -25-30 bp upstream of the transcription start site (article)

This is a quite old article (1995) however inferring the text above signal is more/previously used to describe a TATA boxes near protein-coding genes whereas TATA boxes are more general, so also for non-protein coding genes.

"Box" is an archaic term from long ago. It's little used. "Signal" has now replaced it. "TATA box" and "TATA signal" are synonymous.

Why do you say it is archaic? I hear it frequently and it is still used widely in publications.

I think your are nog right that TATA box is "replaced" by TATA signal, give a quick search on pubMed and you will see that the most recent articles still use "TATA box". Do you have any references for your statement?


text:
Can one refer to pieces of proteins produced by enzymatic digestion as "enzymatic lysates"?
A Russian text I'm translating says this:

The location of post-translational modification (PTM) sites was determined using the “bottom-up” approach commonly used in this field. In accordance with this approach, enzymatic lysates from each of the studied MAB batches were separated using a reversed-phase chromatography column at high pressure (UHPLC), and peptide maps were plotted.

Can one refer to pieces of proteins produced by enzymatic digestion as enzymatic lysates? Or will lysates always imply that a biological cell has been destroyed?
The text I'm translating does not refer to cells being destroyed. The proteins in question are monoclonal antibodies present in drugs (solutions, tablets), therefore no cell destruction is involved.
I'm unsure whether to retain this word, "lysates", or use "digests" instead.
Here's an excerpt from the original Russian text:

Идентификация положений РТМ проводилось по общепринятому в отрасли подходу «снизу-вверх». В соответствии с этим подходом, ферментативные лизаты каждой исследуемой серии МАТ разделяли на обращенно-фазовой хроматографической колонке при высоком давление (УВЭЖХ) с получением пептидных карт.

Digests would ok or maybe hydrolysates. Incidentally for monoclonal antibodies I think mAb, not MAB, is probably standard usage.


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How widespread in the Animal Kingdom is Aromatization as the Process that Determines an Animal's Sex?
I shall summarize my lay understanding of my question before going into details. To my lay reading, the sex of a vast diversity of animal kingdom species can be thought of as arising from the extent that the process of Aromatization - the catalyic conversion of testosterone produced by the gonads to oestrogen - happens. This extent of aromatization can be egg temperature determine, or genetically determined.
The German "Aromatase" Wikipedia page makes the following curious, unsubstantiated claim (translation mine, so apologies in advance):
"Aromatase (aka CYP19A1) is the Enzyme that in backboned animals catalyses the conversion from testosterone to oestradiol ....[emphasis mine]"
Which raises the question in the title. My understanding was that the aromatization process as the sex determining process was wider spread in the animal kingdom than backboned animals, at least as wide as chordates. Since the claim is unsubstantiated, i put the question in my title to this community.
Another take on the question: Can anyone give me examples of animals which are not backboned animals and for whom sex is determined by the extent of the aromatization reaction?

What non-vertebrate chordates do you have in mind? In any case, the claim does not say "only backboned animals" so it doesn't seem like finding a non-vertebrate example would disprove the claim (nor does it say "all" vertebrates).

@BryanKrause agreed. But the naming of a restriction like this got me thinking. I guess there aren't many non vertebrate chordates, but as ascidians spring to mind, for example.  Anyhow, as someone undergoing hormone therapy, the process fascinates me.there seems to be a great deal of lay info on the process in humans, but not to much on fellow animals and indeed how the process cake into being.

I think most ascidians are hermaphrodites (possibly all but I don't know nearly enough to make that statement). If you want to know about sex differentiation more broadly it might make more sense to focus on further flung species that have been well studied, like drosophila, and contrast between humans and flies.

@BryanKrause Interesting. I don't know much about ascidians, aside from that they taste really good, at least the ones on the shores of my home state Victoria do. See also the Japanese dish kenned as "Hoya". See the "other" take on my question. I completely disagree with the Wikipedia description of the taste of sea pineapple BTW - the Japanese and Victorian edible ones taste almost identical and like salted sour cream with a sweet aftertaste, but with a soft meaty texture. Most peculiar but thoroughly ambrosial nonetheless.


text:
How do cats survive falling from great heights?
Among mammals, cats are able to land safely when falling from great heights. For example, when compared to dogs or humans they can survive drops from relative large heights. How do they manage?
A 1987 study from the Journal of the American Veterinary Medical Association. Two vets examined 132 cases of cats that had fallen out of high-rise windows and were brought to the Animal Medical Center, a New York veterinary hospital, for treatment. On average the cats fell 5.5 stories, yet 90 percent survived.
See wiki on cats.
How can cats do this?

insanely good reflexes; too high = broken cat.

I edited your question quite extensively. If it doesn't reflect your intentions anymore feel free to roll back.

I edited the question and vote for re-opening. The reason for question closure (unclear what you are asking) is not applicable any longer as it is edited. The question subject has been hardly researched and pretty interesting.

@ChrisStronks - in a study of 132 cats falling from an average height of 5.5 stories (most: 32 stories), about 2/3 required some sort of medical treatment as a result of their fall, and about half of those that required treatment (1/3 of the total cats brought in) would have died without medical aid.

@anongoodnurse, that makes sense. I wasn't thinking straight...

@ChrisStronks can you add the link to that article?

@WYSIWYG: the Nature paper is linked in the answer. The other one (5-stories falling kitties in Am Vet Med Assoc) was brought up by anongoodnurse and she should hopefully be able to link it in the question edits.

Keep in mind that there's a selection bias issue here: If a cat falls out the window and dies, it's unlikely the owner takes it to the vet. Also, if a cat falls out the window and doesn't look hurt, the owner doesn't take it to the vet. This was explored on the podcast/radio show Radio Lab: http://www.radiolab.org/story/102525-vertigo/

The reason why cats are superb jumpers has not received much attention, but one article in Nature was entirely devoted to just this (Diamond, 1988). Here follows a partly quoted and partly adapted text from this article:
First , because mass increases as the cube, but surface area as the square of linear dimensions, falling large animals are in general more injury-prone than small ones, as they suffer greater impact stress, their bones experience greater stress, and they reach higher terminal velocities in free-fall because of a less favorable area/mass ratio. While a small drop breaks an elephant's leg, a falling mouse reaches terminal velocity in the atmosphere much sooner and at a much lower value than do falling elephants.
Second, falling cats have a superb vestibular system and make gyroscopic turns
such that all four feet are soon pointing downwards, regardless of the cat's
orientation at the start of the fall. Hence cats dissipate the impact force over all four limbs. Falling human adults  tend to tumble uncontrollably but land most often
on two feet, next most often on their heads. These facts contribute to the low mortality of falling cats and to their low chance of breaking limbs after the fall.
Third, a cat falling in the atmosphere reaches a terminal  velocity  of  about  60 m.p.h. (compared with 120 m.p.h. for adult humans) after only  about  100 feet. As long as it experiences acceleration, the cat probably extends its limbs reflexively , but on reaching terminal velocity it may relax and extend the limbs more horizontally in flying-squirrel fashion, thus not only reducing the velocity of fall but also absorbing the  impact  over  a greater  area of its body. This may explain the paradoxical decrease of mortality and injury in cats that fall more than 100 feet.
Finally, cats that land with their limbs flexed dissipate much of the impact force through soft tissue. Parachutists are trained to dissipate impact forces by landing with knees and hips flexed, then rolling.
Reference
Diamond. Nature 1988; 332:586-7
Further reading
BBC news


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What is the significance to life of the anomalous properties of water?
I have heard that the anomalous properties of water - e.g the fact its solid form is less dense than its liquid form - is extremely important. In fact, some people have gone so far as to tell me it was crucial for the development of life.
What is the significance of the anomalous properties of water to life?

This is a brief treatment of your question, specifically:

the fact its solid form is less dense than its liquid form - is extremely important. ...crucial for the development of life.

I can't speak to the importance of this property in the development of life (as I don't know the exact conditions of the world when life began, and therefore the role expansion of ice played in it) but life would not continue without it.
Water does not conduct heat very well, therefore water temperature fluctuates more near the surface of a body of water (say a lake, an ocean, or even a river) than in the deeper regions. In the winter, surface water freezes.
If water were denser on freezing, it would sink to the bottom, and liquid water would replace it. That liquid water would freeze, sink, be replaced, etc.
When it became warmer, the frozen water at the bottom would be less affected by surface temperature, i.e. it would be less likely to melt.
Even with summers, because of the failure of deep ice to melt, eventually you would be left with a mostly frozen body of water, and life doesn't carry on well in those conditions (freezing of the cells of plants and animals in the water would cause cell lysis, again, because of the expansion of water within), whereas life in a liquid under a frozen surface carries on much better. Life in the water would die.
If there were no life in water, then life on land would be most difficult. (Consider most of our oxygen comes from phytoplankton in the oceans. Even if the phytoplankton didn't happen to die from being trapped in frozen water, their nutrient supply would be cut off, frozen below.)
That's just the tip of the iceberg, really. The anomalous expansion of water also affects ocean currents and weather in ways that enrich life on earth.
Since you didn't ask about the other properties of water, this answer doesn't address surface tension, etc.
Edited to add: Corrected an error about the thermal conductivity (insulating properties) of ice. Ice does conduct heat more than water. It may be advantageous to the temperature of the water below possibly by holding snow (which does insulate well).
Source
Thermal Conductivity
Plankton: Ocean Drifters

Nice. I would say that frozen water "contains more air" though. You probably just mean that there are fewer molecules per volume --- lower concentration.  And is this lower concentration really related to insulation?  Does solid water really conduct less heat than liquid water? A reference for this?

@Roland - You're right in all your points. The thermal conductivity of ice is greater than the thermal conductivity of water. I've edited my answer.


text:
How can we know or measure pain in animals?
Is there any standard way to know how much pain an animal feels when it gets hurt like when a bird loses it's wing or hen when killed etc. All pain sensation points?
Hey I'm new to biology. :)

Pain is subjective
Pain is a subjective experience; you cannot even tell with certainty how much pain your fellow human is experiencing, which is why we ask people; they then can tell us. Pain relief (both physical and emotional) is a significant part of medicine, yet we still have "pain scales" for self-reported pain, one of the more common ones being the Wong-Baker Faces Pain Rating Scale:

Now, note well that even this scale must be interpreted for the patients. For instance, a patient might look like a 6, but be reporting a 10, in which case, a nurse must try to ascertain their actual level of pain.
My point is evaluating pain is contentious even in humans who can express themselves.
Definition of pain
The International Association for the Study of Pain (IASP; www.iasp-pain.org) defines pain in humans as

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Pain usually involves a noxious stimulus that activates nociceptors in the body that carry signals to the CNS where these signals are processed (and generate responses) including the “unpleasant sensory and emotional experience.”
The following are examples of common types of noxious stimuli for different tissues:

Skin: thermal (hot or cold), mechanical (cutting, pinching, crushing), and chemical (inflammatory and other mediators released from or synthesized by damaged skin, and exogenous chemical stimuli such as formalin, carrageenan, bee venom, capsaicin)
Joints: mechanical (rotation/torque beyond the joint’s normal range of motion) and chemical (inflammatory and other mediators released into or injected into the joint capsule)
Muscle: mechanical (blunt force, stretching, crushing, overuse) and chemical (inflammatory and other mediators released from or injected into muscle)
Viscera: mechanical (distension, traction on the mesentery) and chemical (inflammatory and other mediators released from inflamed or ischemic organs, inhaled irritants).

Animals need us to interpret their pain into language. For political and emotional reasons, humans are ill-disposed to do so (how could we then justify eating, exploiting, experimenting on animals, etc.). Even into the late '80's, veterinarians were taught that animals didn't perceive pain per se.
How we know animals understand pain
To determine whether animals can experience actual pain (not simply nociception), it is necessary to show that they

can discriminate painful from nonpainful states; make decisions based on this discrimination in a way that cannot arise from evolved nonconscious nociceptive responses; demonstrate motivations to avoid pain; and display affective states of fear or anxiety if threatened with noxious stimuli. In addition, animals experiencing pain might be expected to exhibit spontaneous behavioral changes including sustained signals of distress and impairments in normal behaviors such as sleep.

Animals show all these behaviors. Additionally, there is ample evidence that emotional pain in animals is real. The mere threat of foot shock (electric) induces signs of stress in rats and mice that can be alleviated with anxiolytics (drugs that reduce anxiety).
Even fish show responses to a painful event: guarding behaviors, unresponsiveness to external stimuli and increased respiration, all of which improve with morphine. This is called analogous evidence: evidence that they are, mechanistically at least, directly analogous to pain responses in more complex animals.
Humans are animals
The nervous system of mammals is fairly identical to our own (we are animals). A chimpanzee who is afraid of a pin after being stuck with one 20 times in a row clearly feels physical pain and fear. That a chimp can mourn the death of a parent by not eating and not moving for days clearly indicates that they can experience emotional pain.
In summary:
Pain is subjective. I cannot really tell exactly what you feel if your arm is ripped off (your bird-wing example) or (don't read if queasy type)

 if you are given an electric shock, your throat is slit and, while still bleeding, you are dipped in boiling water to remove your body hair in a whole body hair plucker (which is how most poultry - usually males, not hens, btw - meet their makers).

By definition, only you can tell us.
But common sense and experience tells us it would be painful. And, yes, animals feel pain pretty much exactly like we do. Because we are exceedingly "more alike" than we are "slightly different".
Can animals feel pain?
Pain in Research Animals: General Principles and Considerations
Which Responses Indicate Pain and Which Nonhuman Vertebrates Display Them?<- read this if you really want to know
Evolution of pain

so what about those waveforms which you guys were discussing in this question... http://biology.stackexchange.com/questions/25986/what-does-pain-look-like-in-wave-form

@Wiser - Since it's unethical to experiment on humans, most of the information you read about action potentials and waveforms and such were derived from animal studies and applied to the understanding of human physiology. More proof that we are alike.

@anongoodnurse and since each species is a bit different and extrapolating from mice isn't particularly accurate, most practical data and measurements on human pain (and other) thresholds comes from the (thankfully) few times/places where we did experiment on humans some 70 years ago.

@Peteris - I'm sorry that you believe what you do, but very little of real science came from that period. Probably the most (hideously) useful information is about limits of endurance, not anything more scientific. Also, I would challenge you to refute me with science, not philosophy. We are exceedingly more similar than we are slightly different.

This answer is really solid and well-worked out. +1. I totally agree with @anongoodnurse that, in the end, the only way to guess how another animal species experiences pain, is to assess ones own experiences with a similar noxious stimulus and assume it is experienced similarly by an(y) other animal. I also agree with the similarity between species, as analgesics work pretty much the same for all mammals, at least as far as I know.

We work a bit with pain and memory. My understanding is that you can measure what in behavioral field is called "pain" by detecting aversive response of an animal. That is there is always something unpleasant and attractive in nature. Only difference is that pungent smell will not kill subject. Evolution taught animals that bad smells and loud sounds might bring danger and thus pain, so they try to escape. But pain per se is something that is definitely tissue-damage inducing at some point of intensity. Pain is only signal that tissue damaging influence has approached.
ADD: I re-read your question. There is no way to tell whether or not bird feels pain when wings are cut without anesthesia. Nice experiment would be to rip off human's arms and bird's wings while both are in fMRI scanners or other functional brain imager. If same areas of brain light up, it means that feeling might be similar.


text:
Can swallowed fingermails, hair, or skin get caught in your appendix?
There is a common saying in my place: If you eat your skin, hair or nails, it will be deposited in the cecal (Vermiform) appendix, and can cause appendicitis. (This is mostly told to children to discuourge them from eating their own.)
Is there any reality in this statement? In the case of hair and nails they are dead cells, but what is the issue with skin? Skin is normally living and the cells are active.
So is there any problem digesting ones own skin?
Do nails, skin and hair must be trapped in Vermiform appendix?

Hint: Keratin. Usual proteases in our gut cannot digest keratin.

This is something that Proteinase K can do - hence the name "k".

Most questions in SE are placed "on hold", I think there are straight forward answers exist to this question. Can someone enlighten me, for what reason this question is put on hold ?

Skin is safe to chew, and digestible. Fingernails are not digestible, so really shouldn't be swallowed if avoidable. In the medical literature, there are at least 225 cases of foreign bodies in the appendix. They include:

a metal drill bit that was ingested unintentionally 3 months earlier
pins (81  cases)
lead shot (81 cases)
seeds (34 cases)
bones (16 cases)
eggshell
glass
teeth
nails (hair causes problems with bezoar formation)
a die (dice)
the clinical end of a thermometer.

Most (71%) patients were symptomatic, typically with intermittent abdominal pain for months or years. Pins were most likely to elicit symptoms (93% of cases).
So it seems there is some truth to this nugget of folk wisdom.
The above were found over many, many years. Since most cases are asymptomatic, it's likely there are many cases that never come to light, but not remarkably so (lots of appendices are removed and examined every year!).
Foreign Bodies in the Appendix

What about digestion of skin, WYSIWYG commented that Keratin is indigestible.

@Jvrek - please see the first line.

Wow, it's really kept here for years! How do they send the  little cameras to the digestive track so they get out?

I would have put bezoars in big flashing letters at the top of the answer, as the number 1 reason not to do it... ugh.


text:
Can we determine a person's age by dating methods or other means?
There are many sports restricted to players of a certain age (e.g. 16 and under, 18 and under, etc.) What if a person is older and fakes his birth certificate to say that he is younger? Is there any way to expose this person?
Can we determine such a person's age by radiocarbon dating methods or other means?

Have you read the Wikipedia article? In the very first paragraph it states that the object to be tested must be dead, as it stops exchanging carbon with the environment. So, no.

You'd have to kill them first…

Even if possible C14 dating would not be sensitive enough as the resolution (see wiki: http://en.wikipedia.org/wiki/Radiocarbon_dating#Errors_and_reliability) is about 80 years :)

If you dated a person for long enough, I hope they'd tell you their real age eventually. Sometimes I think biologists should get out more.

No, one can't confirm age by carbon dating. That doesn't mean we can't make a decent guess by other methods.
There is an interesting case of a 33 year old Texas woman who enrolled in 10th grade in Texas. She said she had no transcripts because she had been homeschooled. She looked like a teenager and acted like a one too. She even fooled her new 23 year old boyfriend. So it happens. It also happened in the Little Leagues World Series, if I remember correctly. A twenty-something guy passed himself off as a 14 year old. He was a star (for a while).
In children and adolescents, the combination of a dental exam, dental films and bone X-rays can narrow a one's biological age well. Once the bones are done growing in length, that avenue is closed.
After that, someone might have to provide a tooth. Chemical analysis of tooth dentin, such as aspartic acid racemization, has shown reproducible and fairly precise results.
Global levels of carbon-14 (14C) have been carefully recorded over time. In one 2010 study, forty-four teeth from 41 individuals (one per individual) were analyzed
using aspartic acid racemization analysis of tooth crown dentin or radiocarbon analysis of enamel. Teeth from individuals with dates of birth ranging from 1936 through 1994 (aged 13–70 years) were analyzed, and where the date of birth was known, yielded a 14C-based date of birth estimation accuracy of 1.3 years (S.D. = 0.9 years). In one case, a date of birth was determined to be 1948.4. In another, it was determined to be 1988.

[T]en of these were split and subjected to both radiocarbon and racemization analysis. Combined analysis showed that the two methods correlated well (R2 = 0.66, p < 0.05). Radiocarbon analysis showed an excellent precision with an overall absolute error of 1.0 ± 0.6 years. Aspartic acid racemization also showed a good precision with an overall absolute error of 5.4 ± 4.2 years. Whereas radiocarbon analysis gives an estimated year of birth, racemization analysis indicates the chronological age of the individual at the time of (tooth extraction).

During the course of aging, l-forms of amino acids are transformed by racemization to the d-forms.

[T]he extent of racemization of amino acids may be used to estimate the age of various tissues. Of all stable amino acids, aspartic acid has one of the fastest racemization rates and is therefore the amino acid most commonly used for age estimation....[T]eeth are the tissue of choice for age estimation analysis.

Both methods have strengths and limitations.

The radiocarbon birth dating method can tell the birth date of the person regardless of the time of (extraction). However, the time window for this analysis is limited to subjects born after the early 1940s because the calculations are based on the measurement of bomb pulse-derived 14C.

Clearly this wouldn't be of too much use in people trying to pass themselves off as teens.
Some studies of aspartic acid racemization report accuracies of age ±3 years. The radiocarbon and racemization can further narrow it down.
Why did Charity Johnson pretend to be a teenager for 20 years?
Age Estimation in Forensic Sciences APPLICATION OF COMBINED ASPARTIC ACID RACEMIZATION AND RADIOCARBON ANALYSIS
Strategy for the estimation of chronological age using the aspartic acid racemization method with special reference to coefficient of correlation between D/L ratios and ages

To grab this opportunity to sum up the comments for the C-14 dating method, including those of of @MattDMo and @canadier: Theoretically spoken - Yes we can! But only after (1) killing the person and (2) waiting a few hundred years. As carbon keeps on being recycled in a living carbon-based organism, it has to be dead first. Secondly, because the margin or error is about 80 years, mainly due to the relatively long half-life of C14 (5730 years) and the variability in the C14 dating method (see wiki on C14 dating) one should wait, ideally between 1k and 1000k years. But given the error margin a few hundred years may suffice to get a rough idea. So to sum up - practically this test, although it is objective and free of subjectivity and robust to false pretenses, makes no sense as (a) a human life is about the same a the error margin of the test and (b) the competitor cannot participate in the contest after his or her life has being taken.
I am not aware of any biologoical methods to objectively measure age.


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Texas butterfly with dull underwings, but blue/purple on overwings
I was walking in the grass near the Trinity Trail in Fort Worth, Texas about two weeks ago, and saw these tiny purple streaks flitting about at mid-calf level that turned out to be butterflies.  I followed and tried to get lots of pictures, but the butterflies were quite fast and tiny, and I only got one decent close-up.

Its wings were a dull brown/gray colour when closed, but I couldn't get any better pictures than this grainy one.

Because of how fast it was moving, I couldn't really estimate size reliably, but it was probably slightly wider than the width of my thumbnail when its wings were open.  With its wings closed, the height of the butterfly was about the longest height of my thumbnail.  These are very rough estimates.
It looked quite a bit like the linked picture of a purple moonbeam—one of Google Lens's suggestions—but those seem to be Australian butterflies.

No, not much size variation. Try LYCAENIDAE (gray wings belong to this family as well.) There are smaller ones (called "blues") very similar to gray hairstreaks, e.g.the Echo Blue. Hard to find the distribution, though, but definitely Southern N.A.

@anongoodnurse, thanks!  Google Lens also turned up Echo Blue as a suggestion, but, as you say, I couldn't find information about their geographic distribution, or even a picture like you offer.  The size seems right, so it could be!  Searching also turned up the Melissa Blue, whose overwings look just right, but not the underwings.

@anongoodnurse, re, I think enough time has passed to regard that as the most definitive answer I'll get. If you would be willing to post it as an answer, then I will accept it.

What an odd coincidence: I thought of you today when I saw this video, wondering if it was your Melissa Blue. Thanks for the offer, but I'm disinclined to post a guess as an answer. I hope you understand. :)

@anongoodnurse, re, I do.  Would you mind if I posted it, with credit to you, just so that I can mark this question answered?  Incidentally, I saw a few Melissa Blues this year, and one literally just today! I can't remember perfectly, but this one seems about the same size and overwing colours, just different underwing, so Echo Blue seems likely—and I've almost certainly forgotten any more details than that that some future sleuth might rely on anyway.

Whatever you want to do is fine with me. I agree the underwing is much like a grey hairstreak. I've never seen a Melissa Blue; lucky you!

@anongoodnurse said:

Try LYCAENIDAE (gray wings belong to this family as well). There are smaller ones (called "blues") very similar to gray hairstreaks, e.g.the Echo Blue. Hard to find the distribution, though, but definitely Southern N.A.

Since this was a guess, they said that they preferred not to post it as an answer, but also that it was OK for me to do so, with attribution.  To avoid reputation, I am making this answer CW.
Though I no longer have a perfect recollection of the fine details of this sighting, and only the grainy photograph to jar my memory, I believe, based on later definite sightings, that the butterfly in the pictures above is indeed an echo blue.


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Why do we have such a wide range of responses to pathogens and carcinogens?
I was reading an article recently debunking the idea of 'boosting' your immune system. It occurred to me that - presuming it's right - our immune systems are all pretty much the same (with the exception of the immunocompromised). Given this, I wondered why there is such a disparity in how people respond to pathogens or carcinogens.
Most people would be quite happy, for example, to say that poor food hygiene causes food poisoning or that smoking causes cancer, but in actual fact, most of the time they don't. People who have poor food hygiene standards have them every day, but they're not sick every day, they're sick once in a while. Only 25% of heavy smokers actually get lung cancer, even with something like Asbestos, only 1 in 10 former Asbestos workers actually get Mesothelioma.
What is it that protects most people from these diseases despite definitely encountering the pathogen/carcinogen concerned?
I realise the most obvious answer is the immune system, but that just shifts the question to why this doesn't protect everyone all the time. Presumably the immune system doesn't just have a day off every now and again

It is indeed our immune system. And for cancer it catches most (probably more than 99.9%) of the cells going wild. But still, once in every while one of these cells escapes and causes problems. The same with the stuff in the environment you live in. You are used to it, your immune system is trained on it. Only new pathogens will cause problems. Or you, getting into a new environment.

@Chris. As I said in the question, I'm aware of the role of the immune system. What I'm asking is by what mechanism exactly does it fail from time to time?

This answer will address only cancer.
There is no such thing as standardized exposure to carcinogens in humans; while it would go a long way to answering your question, it would be unethical.
Also, it is unlikely that two people who do consume identical amounts of a carcinogen have identical environments or identical genetics.
Cancer used to be thought of as a carcinogen-host interaction; expose a (rodent, in my studies) to adequate levels of a carcinogen and cancer will occur. We tried to figure out exactly why. Then it was thought of as a host + environment (This was decades ago.)  The immune system was found to play a role; another level of complexity was added.
Mapping the entire human genome has made us aware of how simplistic these (and most) models were. There are tumor-suppressor genes. There are genes that matabolize carcinogens differently from other genes. There are genes that direct repair of DNA better than other genes. The possibilities are just beginning to surface.
To answer your question more directly,

Although many studies have focused on carcinogen metabolism and cancer risk, more recent studies are considering DNA repair.

I would not go so far as to label DNA repair as Immunology.
I don't know why my father, who had a 120 pack year history of smoking, had absolutely no ill effects (not a trace of COPD, and certainly not cancer, no heart disease, CVD or other) and why my mother had COPD at a 40 pack-year history, but I'm sure it was genetic.

Sporadic cancers are caused by genen-environmentn interactions rather than a dominant effect by a specific gene, environmental exposure, or gene-environment interaction. New paradigms, where we categorize genes as caretaker or gatekeeper genes, will allow for new hypotheses to be tested and will require advanced methods of analysis.

And, in another study,

Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes.

Cancer Risk and Low-Penetrance Susceptibility Genes in Gene-Environment Interactions
Integrative Epidemiology: From Risk Assessment to Outcome Prediction
Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)

Thanks for the thorough answer, if I could just ask for clarification on one point. If I understand correctly, you're saying that response to a given dose of carcinogen is a result of - host environment, host immune response and host genetics (discovered in that order). If that's the case, to take lung cancer and smoking for example. Heavy smoking only produces cancer in about 25% of smokers. The genes you've pointed to in your last study give a 35-50% increased risk, that still leaves a huge amount of resistance to cancer unaccounted for, is that correct?

Also, as may be clear from my comments to the last answer, I'm interested in the research into the host response in terms of factors that a host could control. Is the move to genetic studies a result of the general trend in research since the human genome project, or have there been studies actually eliminating other non-genetic host factors?

@Isaacson - Yes, you're correct. There is also the possibility, though, that a cancer-causing mutation will not occur in 100% of the population exposed to a carcinogen. No, none of the other factors have been eliminated, but they have been, say, relatively dwarfed by genetic factors, for example, in breast cancer, the presence of estrogen and progesterone receptors, multiple copies of the HER2 gene, microRNA, DNA methylation, presence of the BRCA1 gene, and mutations in several other important genes. See, e.g. http://www.nature.com/nature/journal/v490/n7418/full/nature11412.html

Intro courses on pathogens often show a triangle representing interactions between host, environment, and pathogen to help explain why outcomes are so diverse.  Each of those parameters is very diverse, so the combination of the three is even more diverse.  At a simple level, you could think about one fit, well-rested person exposed to a low concentration of pathogen, in a warm, comfortable environment, and compare to a stressed, malnourished person in a hot, humid environment, exposed to a large bolus of pathogen.
As well as concentration, pathogens individually vary in their virulence.  Individuals all have unique immune systems, with tremendous diversity (the immune system contains genes that are by far the most variable in human -- or virtually any vertebrate -- populations).  And environmental effects interact with both sides to enhance or reduce susceptibility in many ways.
It's a set of many overlapping complex systems, basically.  Sometimes it's possible to point to a specific combination of causes, but more often we just see a few people getting sick while most remain healthy, and never clearly understand why.

I get most of what you're saying, but your mention of the fit well-rested person seems to suggest that one can, in fact boost your immune system by being fitter, getting rest etc. If that's the case and the figures I mention in the question are accurate, then when people talk about the 'cause' of a disease it would be more correct to say that lack of fitness and stress was the main cause with everything else only secondary.

First, the notion that "lack of fitness and stress was the main cause" is not in my answer; I listed them as among many potential influences, not by any means a main cause; it's telling that you assumed in spite of the phrasing that this is a "main cause", because it ties into a common (misguided) notion that disease has a moral aspect, people get sick because it's their fault, it's a punishment, and recovery is a sign of virtue.

More importantly, it's not a question of "boosting" immunity. People have a normal default level that can be damaged, not a normal level that can be boosted.  You can, to take an obvious example, take immunosuppressive drugs, like catabolic steroids.  Among that common causes of mild to moderate immune suppression, lack of sleep is one well-supported cause; morbid obesity another.

My intention was not to make a moral point, but a statistical one. It's like saying a runner won the race because he turned up. Turning up was certainly a requirement, but it's not why he won because other runners also turned up and they did not win. The thing we ascribe as the cause is what sets that runner apart from the others. I don't see why the same is not true when we ascribe a cause to disease.

The moral point that I would make though is this. If you drive, there is a chance you'll be killed on the road, but engineers do not simply say that driving kills people and leave it at that, they look at each individual case and try to work out what happened and how they can make it safer for others - seatbelts, airbags etc.

Medical research, however, seems to find a generic cause and then leave it at that. Lots of people are, to use my examples above, exposed to asbestos, passive tobacco smoke or poor food hygiene inadvertently. It's no help to these people to say that these things are dangerous and should be avoided. What would help is if they knew how they could ensure they were part of the majority who are exposed to these things and survive, not the minority who don't.

I'm not sure what your issue is.  I tried to indicate that the interactions between host, pathogen, and environment are extremely complicated.  You promptly claimed that "lack of fitness and stress was the main cause", which is exactly the opposite of what I said, and then you're accusing me of oversimplifying and focusing on a generic cause.  As far as looking for why most survive, that is an intense field of research, but I'm not particularly interested in trying to explain it to someone who is trying to hard to force my answers into their own personal agenda.

If you read my comment I'm accusing the medical establishment of focusing on generic causes not you. For evidence, look at the NHS website on lung cancer, mesothelioma or food poisoning (the examples I've used above), any mention of stress, fitness, lack of sleep among the causes? Yet, as you say in your answer these are important factors, hence a perfectly rational conclusion that they are under represented by the medical establishment.

Nonsense.  I'm as much a part of the "medical establishment" as anyone, and I just quoted the consensus opinion in the answer you agree with, so you're obviously wrong.  As I said, my answer is the typical introduction from the very first courses on pathogens, and it's such basic, common knowledge among the "medical establishment" that to argue it's somehow obscure and unknown means you've never even taken the basics, so you can hardly make claims about what they do and don't know.

Please read my comments more carefully before replying. I'm not making any claims about what they do and don't know, I'm talking about what they do and don't say to the general public and I've provided evidence to justify that claim. I've also provided comparative examples from other fields regarding the way people generally use the term "cause", which I think is significantly different enough from the way it is used by the medical establishment to require an explanation. All I have done here is ask for such an explanation, I have yet to receive one.


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What is regional homogeneity in neurology?
newbie to.neurology here. For context, I'm studying this article (https://www.nature.com/articles/s41598-021-89166-8#Sec14) which relates the gut microbiome to brain structure in schizophrenia patients. The paper uses the term "regional homogeneity" so often throughout the paper without explaining what it means, and my attempts to research it only leave me more confused. I only understand it as some measure of
brain activity with other stuff related to synchronization. That's kind of a problem since so much of my project depends on knowing what it means exactly. Any help is greatly appreciated.

4th paragraph of the introduction (Alterations in brain function...) and the 4th paragraph of the method section titled "MRI data collection and preprocessing" (The ReHo index was calculated...) tell you what it means. You probably need to read the cited references for a deeper understanding, or at least search Kendall's coefficient of concordance.

@anongoodnurse Then one needs an explanation of voxel and connectome, not regional homogeneity. Regional homogeneity similarly can be simply understood from the separate meanings of those two words, but what's relevant for this paper is how it's calculated which is very clear in the methods.

@BryanKrauseisonstrike: Thank you for pointing me in a general direction, but I can't afford to go down the rabbit hole of researching and understanding what functional connectivity and friends mean. Do you understand this concept at all, and if so, would you be willing to walk me through it?

@Specs_Goldfish Hi, I'm sorry, but, your comment is not correct. In fact, you can't afford not to go down that rabbit hole if you want to use this technique for anything at all. Your project depends on you going down that rabbit hole, and really, understanding functional connectivity at least at a level sufficient to understand this technique is not a "rabbit hole", it's one of the principal methods used to study human neurobiology. Ignoring it would be like leaving telescopes out of astronomy.

@BryanKrauseisonstrike: You're right, I absolutely need to read everything to get a formal understanding, but for a dense high school student with a presentation due in two days, any sort of oversimplified explanation will do. I apologize for showing up so unprofessionally.

@Specs_Goldfish I'd start with at least the Wikipedia article on resting state fMRI. You might also search "functional connectivity" here or on Psych & Neuro StackExchange. Taking shortcuts due to a short deadline is a strategy you should quickly learn to avoid - one strategy is to be better prepared further in advance of the deadline.

You state, "...my project depends on knowing what it means exactly..." Then you need to know exactly, which can't be explained in a couple of sentences. You're asking professionals to help you out of a jam (a time crunch) that you created for yourself.

Good question! The brain is composed of billions of cells, and not all of them are doing the same thing at the same time. Some areas of the brain may be more active than others at any given moment. However, within specific regions, the cells (or neurons) are expected to be working together -- or, in other words, they should be synchronized.
When we use fMRI to scan the brain, we're creating a 3D image, and each tiny cube or box within that 3D image is called a voxel. I.e., "volumetric pixel," just a box instead of a square like a pixel. Each voxel represents a tiny portion of the brain, containing a large number of neurons. In an fMRI scan, the intensity of the signal we receive from each voxel can tell us how active that part of the brain is (based on, for example, how much blood is being used in the region).
ReHo is a measure of how similar the activity is within a cluster of voxels. If they are all behaving very similarly — if they're all increasing or decreasing their activity at the same time — then we say they have high regional homogeneity.
To calculate ReHo, we use Kendall's coefficient of concordance to tell us how well the activity across a cluster of voxels is synchronized.
You can imagine that some disorders would disrupt brain connectivity/communication between neurons, resulting in more disorganization. Or you could imagine that excessively high ReHo might indicate some altered state of mind.

From my reading, your answer is correct but very simplified. I don't know just how much detail the OP needs (for example, how much volume is in a voxel, and approximately how many neurons in that voxel, how many voxels in a cluster, and how Kendall's coefficient tells us how well activity in a cluster is synchronized.) But what I really don't understand is your last sentence. I think you need to provide some support for it. Thanks.


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Which requirements are needed for 2 different species to be able to have offsprings?
Sometimes different species mate and they are able to have offsprings, usually with anomalies. Are there known requirements for 2 different species to produce offsprings? Why species like the lion and the tiger, which seems to have many differences are able to produce offsprings, when others which supposedly share 99% of the DNA can't?

Lets break this down like a logical problem. In reality, it involves the correct gene expressions at the correct time, place, etc. But that would be a book.
Prezygotic reproductive isolating mechanisms
Environment
A bull and a whale can't mate; they don't live in the same environment. Lions and tigers similarly do not mate in the wild due to lack of overlap in the environment. In captivity, yes.
Delivery of gametes
Sperm must be able to be delivered to the ovum for fertilization to occur. Some species just can't get this part right. Your house cat would not be a suitable donor for an elephant.* In closer species, say a chicken and a peacock, the rooster's courtship display (which is nowhere near as spectacular at the peacock's) will not be accepted by the female; no opportunity for delivery of gametes.
Some gametes can be delivered but not ova (the female isn't "in season".) Zero there as well.
Unity of gametes
If the gametes are both delivered at the correct time, can the sperm bind to the egg? Successful binding requires a receptor-ligand interaction which actually has a high degree of species specificity. So binding requires that the sperm and the egg can, say, "communicate" successfully. Dog sperm doesn't "speak" cat ovum.
If they do "speak the same language", can the sperm penetrate the ovum's protective coating (the zona pellucida)? Assuming sperm capacitation (a big hurdle right there), the sperm may not have the correct enzymes in it's 'head' to penetrate zona pellucida. Not all enzymes carry out the same function on all molecules, and if the correct enzymes are present to digest/break through the zona pellucida, is there enough? Is the sperm active enough? I'll liken this kind of communication to 'pillow talk'. We're getting much closer. Let's say the sperm has his pillow talk down, and can penetrate the layer.
Postzygotic isolating mechanisms
Viability
The hybrid embryo must be able to develop into a zygote. Hybrid inviability means there wasn't enough similarity to proceed to a blastocyst and the hybrid dies.
Say viability is achievable. The blastocyst/blastomere must "communicate" with the mother so that attachment is not only possible but can be sustained. In effect, it must "shout" to the mom, "I'm here! Pay attention to me!" (In humans, this involves secretion of large quantities of a hormone called chorionic gonadotropin, which stimulates continued secretion of progesterone, thus no shedding of the uterine lining. Not all mammalian blastocysts communicate the same way. If what we have here is a failure to communicate... as with Cool Hand Luke, the result is not good.
Hybrid sterility
The species were close enough for the conceptus to be heard by the mom. The right chromosomes with the right gene expression results in a live birth.
Success!
If the hybrid is fertile, it is by one definition not a different species. (There is much debate as to what exactly defines a species. See the references.)
If you are still left saying, "But why?", then it must be explained on a genetic/molecular level, with sentences like,

The zona pellucida of mammalian eggs is composed mainly of three glycoproteins, all of which are produced exclusively by the growing oocyte. Two of them, ZP2 and ZP3, assemble into long filaments, while the other, ZP1, cross-links the filaments into a three-dimensional network. The protein ZP3 is crucial: female mice with an inactivated ZP3 gene produce eggs lacking a zona and are infertile.

If this is the level of explanation you seek, there's a book for you: Molecular Biology of the Cell. Alberts B, Johnson A, Lewis J, et al.
Fertilization
The Process of Speciation
Fertilization
*Note here I'm referring to morphological differences, one way used to define species.

@BryanKrause - I realize that this is in a bit of flux. Also, I know that there are different definitions of "species", but there aren't any definitive answers, so I simplified a bit, relying on Ol' Faithful... One can say, because of fertile hybrids that they are subspecies like Drosophila ssp. that can have fertile offspring that becone infertile after a couple of generations.... And so on.


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Janina kolkiewicz who faced Lazarus phenomenon
I've just read about Janina kolkiewicz case who faced Lazarus phenomenon and I was wondering how could her brain and organs survive these long hours without oxygen?

How far did you get looking for this answer yourself?

Your question is unclear as it assumes knowledge of a case involving a particular person. You can assume knowledge of biology, but not of this sort of thing. You must describe it and give references.

Without oxygen, she would not have survived. Granted, she didn't need a lot in her reduced metabolic state.


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Do all nerves in the body end at the tongue?
I saw this someone but have  searched on google to affirm or deny it, but didnt find anything on all nerves ending in the tongue. Please help

No, nerve endings are where they communicate with muscles (motor nerves) or the ends are where information is sensed, like touch or taste (https://en.wikipedia.org/wiki/Free_nerve_ending).
You could probably say that all nerves start in the brain but they spread out and end everywhere. http://www.innerbody.com/image/nervov.html

No all nerves do not innervate the tongue.
Out of the 12 pairs of cranial nerves only three nerves innervate the tongue; the pharyngeal part of the tongue is supplied by the glossopharyngeal nerve (IX) and the oral part is suppled by the lingual nerve [a branch of the mandibular branch (V3) of the trigeminal nerve (V)] and by the chorda tympani [a branch of the facial nerve(VII)]. Apart from them the intrinsic and extrinsic muscles of tongue is supplied by Hypoglossal (XII).
The rest of the eight nerves along with C.N IX, V and VII have different extracranial destinations.
For e.g.- The first cranial nerve originating from olfactory bulb of fore brain reach the olfactory mucosa in the upper part of the nasal cavity.

P.S. To understand the extracranial course of cranial nerves read this wikipedia page.
Besides here's a diagram that roughly illustrates the major areas of innervation of Cranial nerves.