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What is the field of view for the human eyes?
I'd like to know how much a person can see regarding the angles.
If it is a rectangle, I'd like to know it's height and width.
But if is another shape, I'd like to know which kind of shape and the angles.
I suppose that we can see something like this and if this is true I am curious about 4 dimensions:

"vertical" angle for both eyes
"horizontal" angle for both eyes
"vertical" angle for an eye
"horizontal" angle for an eye

It would be also nice if there will be some "areas" with percentages. I mean, something related to "central" vs "peripheral" view, because we see better something that is in front of us than something that is near us.

The general shape of the field of view has been answered in the related question "If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?"
Regarding the central view: yes, foveal view has a higher acuity than peripheral view.
Regarding the numerical dimensions of the monocular and binocular field of view: Monocular field of view  (measured from central fixation) is 160 deg (width w) x 175 deg (height h). The total binocular field of view is 200 deg (w) x 135 deg (h).
The region of binocular overlap is 120 deg (w) x 135 deg (h) (WebVision). The binocular foveal high-acuity part (central view) is about 6 degrees (5-15 degrees).

Chris what does the w signify in the brackets? Does it stand for width and h for height? Or does h stand for horizontal and w meant for vertical?

w x h = width x height, question edited. thankx

Good answer so +1. Though it would be more useful if you can split the monocular vision angle in horizontal direction as nasal and temporal fields

@CRags - the linked question covers nasal/temporal aspects. And thanx :)

Sorry, I didn't check that question Chris

One thing that's interesting is that the optical system is not just encoding image feature details (like a camera), but also has built-in low-level filtering that can detect motion with reduced latency compared to the pathway used for feature detection.  This is relevant when considering vision as an ongoing process, since the eyes are typically constantly moving, with a choice of focal point partially motivated by motion detected in the periphery.


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Molecular biology - fundamental questions
Basic Gene, Chromosome, Genome, Protein - how are they ordered?
Genes make up Chromosome, and Chromosomes make up a Genome...
So, where does Protein come into play?
What do you call Genes that are spliced together to form something new?
What do you call a variable inside a Gene?
Thanks.

Welcome to SE! At Biology SE we appreciate some evidence of personal effort of the PO to answer the question. Without it, we may put the question on hold, giving you the chance to add some background information.

I have zero biology education and I am asking because the people that write stuff about such things are very verbose (needlessly so, just like writers for other things) when I just need a quick answer. I am in a circumstance where I must/should get this right. If you have a "for dummies" simple introduction link/answer that can answer the questions, then please post it.

Makes sense. Hope my answer helps.

where does Protein come into play?

A Gene codes a protein.
DNA is transcibed into messenger RNA (mRNA). mRNA is translated into protein.

What do you call Genes that are spliced together to form something new?

Genes are not spliced together. One single gene can consist of introns (intervening sequences) and exons (expressed sequences). Transcribed introns in the RNA are spliced out and the exons glued together to form a functional mRNA.

What do you call a variable inside a Gene?

Genes are made up of DNA. DNA is made up of nucleotides.

+1 Just an interesting note (definitely an exception to the rule), in some organisms, exons from different primary transcripts from different genes can be ligated. This is known as trans-splicing.

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What does it mean when a patient suffering from malignant tumor (cancer) has been declared cured?
Comment by Anongoodnurse, has made me curious as to what a doctor means when (s)he says "The cancer is cured" to a patient.
My idea up till this point (based on what I read and what I learned in my classes from my professors) was that the prognosis was declared based on the survival rates and that cancers could never be declared cured as no one could be sure that every single malignant cell has been eradicated.
However Anongoodnurse commented:

Curable cancers are not few and far between.

So I would like to know what it means when it is said "Cancer is cured"

Though the answer by Anongoodnurse has been accepted, I would like to have other answers too, please feel free to contribute

Being a programmer and not a medical practitioner, most of my knowledge on this subject can be summed up in this XKCD comic.

Lol, excellent one

TL;DR - ask someone who has survived 45 years after treatment of their testicular cancer. The patient (and most doctors) would consider that a cure.
I believe the kxcd cartoon explains prognosis quite well. There is something that @Crags has overlooked, though, and that is the caveat "Once most cancers spread out into your body, they're incurable".

I would consider that sentence to be quite correct. A good prognosis is very different from a cure. Most of the surgeons, radiation therapists and oncologists I have worked with make that distinction. (Even surgeons, whose mottoes include "A chance to cut is a chance to cure." and "Nothing heals like cold hard steel." are careful not to use the word cure, unless it is a cure.)
I am not an oncologist, but oncologists do write papers. From one of them:

METHODS: We analysed postmenopausal women with localised invasive breast cancer. The primary endpoint disease-free survival (DFS), and the secondary endpoints time to recurrence (TTR), incidence of new contralateral breast cancer (CLBC), time to distant recurrence (TTDR), overall survival (OS), and death after recurrence were assessed... FINDINGS: At a median follow-up of 100 months (range 0-126), DFS, TTR, TTDR, and CLBC were improved significantly in the ITT and hormone-receptor-positive populations.

Although this study only followed patients for 100 months (8.3 years), some studies are much longer, and a cure is what you or I would think of as a cure: disease-free survival, not of months, but for a lifetime, that is, non-recurrence of the cancer.
Your professors sound like they are using the standard approach to cure, which is to hedge one's bets:

In medicine, a disease is considered cured when it’s been successfully treated and does not return. The concept of “cure” is difficult to apply to cancer because undetected cancer cells can sometimes remain in the body after treatment, causing the cancer to return later (referred to as a recurrence or relapse). Many cancers are considered “cured” when there is no cancer detected five years after diagnosis. However, recurrence after five years is still possible.

In the past, cure was defined as 5-years cancer free. We now know that that is survival, not cure. The same can be said of 10 years (thought that one runs more true to cure). The fact is, most studies don't follow patients indefinitely. That doesn't mean no cancer is "cured". The patients (even many of those in the xkcd comic) without recurrence are cured. Therefore it is a fallacy to say cancer can never be cured. Semantics and statistics are at play.
As I said in my comments, there are curable cancers.
Curable cancers: non-invasive basal cell carcinoma:

Nearly every basal cell cancer can be cured, especially when the cancer is found early and treated.

(This is not a hedge. The authors are lumping aggressive BCCs in here with the less aggressive BCCs.)
Certain early prostatic cancers:

These results suggest that a patient has a high likelihood of biochemical cure after treatment for prostate carcinoma with conventional doses of external beam RT if he has not demonstrated biochemical failure within 5 years of treatment. Patients with lower pretreatment PSA levels and lower Gleason scores may require longer follow-up than those with less favorable characteristics to achieve the same certainty of cure. Patients who achieve a PSA nadir ≤ 0.4 ng/mL and require ≥ 2.0 years to reach this nadir have the highest probability of cure.

Cervical cancer:

Early cervical cancer can be cured by removing or destroying the precancerous or cancerous tissue.

Colorectal cancer:

Conclusion: Patients who survive 10 years appear to be cured of their disease, whereas approximately one third of actual 5-year survivors succumb to a cancer-related death. In well-selected patients, there is at least a one in six chance of cure after hepatectomy for CLM. The presence of poor prognostic factors does not preclude the possibility of long-term survival and cure.

Childhood acute lymphocytic leukemia:

Impressive improvements of survival rates in pediatric acute lymphoblastic leukemia (ALL) have been achieved during the last decades.1–21 Today, a long-term cure can be attained for approximately 75% of patients.

(Although good survival rates - defined by *event free survival - are defined at 6 years in this paper, there are papers which follow to 15 years with little change in the group. Like most studies, longer times mean more patients are "lost to follow-up".)
It goes on and on.
Finally, my comment was an admonition to you to be wise with your words, not an absolute.
Understanding Statistics Used to Guide Prognosis and Evaluate Treatment
The cure of cancer: A European perspective
Basal cell carcinoma: Diagnosis, treatment, and outcome
Cervical cancer
Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95

Thanks for the detailed explanation. I understand that the confusion is because of the interplay between statistics and semantics. But I gather that a cure seems mostly a retrograde statement rather than a prognosis given at then end of treatment

Or rather a prognosis based on statistics and confirmed only by the passage of years

You ignore the obvious. Some cancers, including BCC and cervical cancer, are curable. If you don't want to accept that, you don't have to. You can believe that a localized cancer which is completely removed will recur in the future. Who can prove you wrong? (Except for the millions who are still alive 40 - 50 years out, and who knows about them, really?)

While what you say is correct, what can you tell about those in whom it does recur, those millions who are in their graves? Then again dead men tell no tales!

Find me papers on the death rates of localized small BCCs. I found papers supporting my answer.

I am stating the obvious, that cure can be pronounced only on retrograde analysis on a case by case basis unless there are cancers with absolutely no chance of recurrence (0 % recurrence rate proven). I mean even if recurrence rate is say, only 0.1% that person could be you.

I am not disagreeing with you, as I said earlier. Just stating the obvious

If you know all the answers, why bother asking the question? You asked "what (does) a doctor mean when (s)he says 'The cancer is cured' to a patient.?" I'm a doctor. I explained it. That's all I'm going to say.

OK, I accepted your answer right? I guess it is subjective, based on doctors too. I agree that you represent a class of thought among doctors. And some cancers do have very low recurrence rates. But it is never zero.

As I mentioned, even among doctors different classes of opinions exist. That was the reason for my question

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How can a plant become resistant to glufosinate?
From Wikipedia, the mode of action of the non selective herbicide Glufosinate is:

Phosphinothricin is an glutamine synthetase inhibitor that binds to the glutamate site. Glufosinate-treated plants die due to a buildup of ammonia and corresponding decrease in pH in the thylakoid lumen, leading to the uncoupling of photophosphorylation. The uncoupling of photophosphorylation causes the production of reactive oxygen species, lipid peroxidation, and membrane destruction.

Now, in this article from the University of California (Weed control, management, ecology, and minutia), it states:

Researchers in Malaysia reported a few years ago on a population of goosegrass resistant to glufosinate in vegetable and orchard systems (Lee L J & Ngim J (2000). A first report of glyphosate-resistant goosegrass (Eleusine indica (L) Gaertn) in Malaysia. Pest Management Science, 56, 336-339).  For a number of years this was the only reported case of resistance to this herbicide.

What would have to happen in the weed for it to become resistant to this chemical/mode of action, and what would initiate this process?

Can you add real citations (Author, year, journal, volume, page) or links to the PubMed (or where ever this can be found)? Than we can have a look at the articles without having to find them first.

I think a general resistance strategy is to pump the offending molecule out of cells. I don't know if that applies here, but I wouldn't be surprised.

@Chris still looking for those

Phosphinothricin is a metabolite from the bacteria Streptomyces viridochromogenes which has a protein called phosphinothricin N-acetyltransferase (PAT). This Protein inactivates the phosphinothricin which is the reason why S. viridochromogenes is not dying from it. If you want a plant to be resistant to phosphinothricin you can add the gen for the PAT protein to the plant genom.
This is also described in this paper about herbicide-tolerant crobs.
An explanation for the resistant goosegrass could be that somehow it got the gen for PAT, maybe by horizontal gen transfer from S. viridochromogenes.
In your case the publication which is cited in your source contains another possibility. "We hypothesize that reduced herbicide translocation is responsible for resistance to both glyphosate and glufosinate in these populations"

Yes, this looks to be correct. Mind adding a reference or 2 before I accept?

I learned this in university this semester, but I'll try to find the publications :)
There could be other explanations to your question


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Why is it important to study chromatin to understand cancer?
Many labs and many projects in biology institutes and university departments have been starting to study chromatin. Chromatin states, chromatin interactions, chromatin loopings, chromatin behaviours, etc. seem to have become the new priority of cancer scientists.
I'm new to this field so there are many things that I still have to understand about chromatin and its relationship to cancer. These questions just flowed into my mind:
What is the relationship between chromatin and cancer?
In cancer research, why is it so important to study chromatin and how chromatin loopings form?
What do scientists would like to find out about chromatin when they investigate it?

This is a very very broad question. Generally speaking chromatin is condensed DNA wrapped around histones and held in place by different proteins, which control what sequences of DNA get exposed or unexposed to transcriptional enzymes. This affects what proteins get translated and what doesn't. Depending on what proteins are translated affects everything about a cell and its survival/metabolism.

Another thing, it is extremely important in the process of mitosis and meiosis in cells.

In cancer cells one of the main microscopic feature is nucleus: cytoplasm ratio. When a cancer cell is stained, it is seen in most cases that this ratio is increased as compared to a normal cell. Mitotic figures are seen much more than in normal cells. So this is another reason why chromatin are studied

I'd read through Watson's "Molecular Biology of the Gene" (7th ED) section on chromatin, nucleosomes, and it's regulation. Then, read The impact of chromatin in human cancer: linking DNA methylation to gene silencing, and Chromatin remodeling and cancer.

Most cancers involve, in addition to genetic changes, a whole suite of epigenetic changes that orchestrate changes in transcriptional profiles. Additionally, multiple epigenetic modifiers (Eg - EZH2) are associated with worse prognoses.
There is also the fact that chromatin modification machinery is very highly mutated in cancers; examples include EP300 - a histone acetyltransferase, and members of the SWI/SNF nucleosome remodelling complex. The study of epigenetic factors needed for the continued transcription of oncogenes like Myc has also led to the formulation of potential therapeutic strategies (Check out some of the literature on inhibiting Brd4 to silence Myc in certain settings).


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How do you determine if donated, stored blood is viable?
Think about stored donated blood; What should we check before transfusing it to a patient, to see if blood is still viable?
What methods to use?
What components should it have in what levels, to be counted as viable?
Detailed version of the question, including some background:
Since I'm a software engineer I'm not aware which kind of topics should I search to find answers that I need. Of course I have tried to find publications and books related directly to this topic. But I could not find any. What I need at the moment is some material to do "some reading/research". And of course, if possible (which I don't know if there are too many possible answers or not) direct answers would be extremely helpful.
Of course I have done some research on indirectly related topics. For example; I have read papers about results of blood storage on blood quality etc. But these papers just analyze the effects, while it is not clear for me if these analyzed materials represents viability of blood.
For more detail, things those analyzed in few papers that I have read are;

CBC: The CBC consisted of 10 parameters: white blood cell (WBC) count, red blood cell (RBC) count, hemoglobin (HGB), hematocrit (HCT), mean cell volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW), platelet (PLT) count, and mean platelet volume (MPV).
Differantial: consisted of relative percentages (%) and absolute numbers (#) of neutrophils, lymphocytes, monocytes, eosinophils, and basophils.
Reticulocyte: The reticulocyte enumeration consisted of relative percentage (retic %) and absolute number of reticulocytes (retic #), and immature reticulocyte fraction(IRF).
The NRBC: enumeration consisted of NRBC per 100 WBC (NRBC %) and absolute number of NRBC.
Others: Factors V, VII, VIII, X, and XI, protein S (PS), a2-antiplasmin (AP), and fibrinogen; and the activated partial thromboplastin (APTT) and prothrombin (PT) times. Factors VIII and factor IX.

Still, I'm reading about each of these. What I'm in need is someone help and say; like:

"You are totally lost, these are not related to your case"
"You should check this paper which is related to your case"
"This, this and this ones in your list are what you are looking for. Focus on them."

Thanks

Have voted to reopen. Great job on sharing your research. A question (which will help direct the answer): why do you want to know this? You've listed some of the normal parameters of blood, many of which have nothing to do with viability.

I'll work on new blood testing techniques for viability. While I'll be working with people from health area, first I want to learn about this topic myself, with my researches. I have been looking for sources on such topics but could not find a solid lead.

Blood can be stored as whole blood or packed red blood cells. The constituents of each are different. Which one will be used varies based on the patient, the availability and the situation. Whole blood (not necessarily warm) is used more often when there is massive blood loss, as it contains all the components of blood: clotting factors, platelets, plasma, etc. Packed red blood cells have had the white blood cells removed, most of the plasma, the platelets, etc. It is indicated for routine blood loss and to increase the oxygen carrying capacity of blood. The constituents of each are different.
The primary problems of stored blood viability are red blood cell deformability (red cells are normally very flexible in order to pass through capillaries) and red blood cell fragility (this results in fewer RBCs actually active in the recipient, as RBCs will break apart.) The viability of RBCs in storage depend on factors such as adequate ADP (the energy substrate). When RBSs are less viable for any reason (less deformable, more fragile, or hemolysis has started in the stored blood), this is termed red cell (or red blood cell/rbc) storage lesion.
Though there are probably many questions you may have about storage methods and viability, this will give you an idea of search terms for your reading. Good luck in your research efforts.
Fresh Warm Whole Blood (FWB
2012 Clinical Practice Guide on Red Blood Cell Transfusion
Blood Products
Deformability of stored red blood cells. Relationship to degree of packing
Microvascular perfusion upon exchange transfusion with stored red blood cells in normovolemic anemic conditions
Studies on the preservation of human blood. II. The relationship of erythrocyte adenosine triphosphate levels and other in vitro measures to red cell storageability
Nitric Oxide Scavenging by Red Blood Cell Microparticles and Cell-Free Hemoglobin as a Mechanism for the Red Cell Storage Lesion
Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy


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Which biosynthetic pathways take place in the plastid and were are they located?
I know that the isoprenoid, jasmonate, glucosinolate, fatty acids, chlorophyll, starch, and aromatic amino acid syntheses are located in the plastid. But I don't know if they are located in the thylakoidlumen or in the stroma.


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Why there are two rounds of cytosine de-methylation in mammalian development?
I assume that the key biological meaning of cytosine de-methylation during germline development in germline progenitor cells is to reset imprinted genes and then set methylation pattern on these genes according to the gender of the embryo. (this is simply my best guess, so if there is an alternative interpretation, please mention it in the answer)
This de-methylation procedure is dangerous, because DNA-demethylation affects a lot of different regions and some transpons get de-repressed. So there is a risk of novel transposon insertions. However, since it is important to set imprinting in your own gamets properly, the embryo takes this risk.
But I don't understand why does de-methylation in mammalian development happen twice. Well, the first round it is not as deep and, I am guessing, that the transposons are probably not affected very much during the first round, so the risk of novel transposon insertions is not as high. However, since the resetting of imprinting marks is happening in the second round anyway, why does the embryo bother the first time around at all?


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Why scientific names of animals & plants are made difficult to spell & remember?
Why scientific names of animals & plants are made difficult to spell & remember?
Mango: it is easy to spell.
Corvus splendens: it is difficult to spell

It's not difficult to spell if your an 18th century naturalist who speaks Latin.

Take the cat: felis domesticus - domestic feline. Take it to a slightly higher level, wolf: canis lupus - lupine canine("lupine" as an adjective ultimately originates from Latin).

I'm voting to close this question as off-topic because this is childish and not about biology in terms of SE Biology.

The reason scientific names are difficult to remember is because the scientific names are given in Latin. There are rules to be followed when naming a organism. That the name must be in the form of Genus species is one of those rules.
For a person who knows latin, it would be just as easy as the English names are for a English speaking person.
In earlier days, Latin was considered the language of the scholars. That was the reason Latin was chosen for binomial nomenclature. As scholars of all languages learned Latin, just hearing the name would give the hearer an idea of what the organism is even if (s)he had not seen it in person.

For more on scientific naming and rules while naming see:

https://en.wikipedia.org/wiki/Binomial_nomenclature
http://education-portal.com/academy/lesson/binomial-nomenclature-definition-classification-system.html
http://www.curioustaxonomy.net/rules.html

The thing is that there is such a language called Latin that is used to name species. During Linnaeus' times when he created the binomial naming system, Latin was the prevalent lingua franca among international scholars. Therefore, all the species names actually make sense, though only hardly so in English.
Names that make a little sense in English include:

Wolf: Canis lupus - Lupine canine
Domestic cat: Felis domesticus - Domestic feline
Wild horse: Equus ferus - Feral equine

These make sense because many English words originate from Latin, be it directly or through French.
Some of the words used in binomial names are Latinization of Greek words (that there are not such words in Latin itself), or valid Latin words that originally came from Greek, so some names would also make sense in Greek. Besides some English words also trace back to Greek.

Lion: Panthera leo - Latin word which originated from Greek
Megalania - Latinization of Greek neologism "mega"+"elaino" = "Great roamer"
Baker's yeast: Saccharomyces cerevisiae - Latinization of Greek "sacchar" + "myces" = "sugar fungus"
Penicillium chrysogenum - Latinization of Greek "chrysos" + "genos" = "Gold maker" as it produces a yellow(golden) pigment

Beyond those are names coined after locations and discoverers:

Flores man/hobbit: Homo floresiensis - Latinization of the location of discovery, Flores
Common kingslayer: Malo kingi - Latinization of the name of the victim, Robert King, whose death by the jellyfish's venom led to its discovery (note that the English common name also came from the name of the victim)

Some species are also named with Latinization of words in other "native" languages, such Panax ginseng, named after the Chinese name 人参 (I'm not sure exactly what dialect/topolect it is).

Beyond species names, Latin is also used in other parts of biology such as anatomy:

Biceps femoris: Two-headed muscle of the femur
Vena cava superior: Upper hollow vein
Corpus luteum: Yellow body (body as in object)
Ileum: Guts/intestines

Beyond biology, Latin is used in meteorology to name clouds, astronomy as the common name of stars (Bayer designation), and remains an official language of the Holy See (the authority of the Vatican) as well as the motto of many organizations:

Cirrostratus fibratus - fibrous layered cirrus(curly hair) cloud
Sirius: Alpha canis majoris - Alpha (number one) star of the constellation canis major
Old motto of USA: E pluribus unum - "Out of many, one" (signifying unity among states)

The question bares a resentment to awkward sounding Latin names. It is unfortunate, since there is surely logic in Latin nomenclature.., but admittedly  it is also unfortunately a steep learning curve to learning some Latin. Anyway, having one gold standard nomenclature, no matter how stupid it sounds, is a blessing for scientist of the field (it's coming from a genomics-ist dealing with alternative gene names on a daily basis where there is no Latin-like-gold-standard and alternative databases compete for rightfulness of their logic and nomenclature). I work on a protein called Mili, and in dozens of papers it is called so, but I cannot guess without googling how it is called in RefSeq or Ensemble power houses of genomic annotations

Scientific names look complicated because they are written in Latin yet English speakers attempt to pronounce them following their language's rules.
In actuality, Latin and its derived languages (such as Spanish), have very straightforward and simple rules regarding pronounciation. Each sound generally corresponds to one character only, which does not happen in English.
The following are some pronounciation rules of Latin.

A is always pronounced as the A in "Ant".
E is always pronounced as the E in "Entity".
I is always pronounced as the I in "Ignorant".
O is always pronounced as the O in "Obelisk".
U is always pronounced as the double O in "tOO".
There are no silent vowels.
There are no silent consonants, to the exception of H, which is always silent.
K and W are not used.

With these rules in mind, read out loud Caenorhabditis elegans. As you can see, its original pronounciation is very simple, but the English one is not.
This is because Latin uses 23 characters to represent 23 sounds, while English uses 26 letters to represent 40 sounds. Many characters in English represent different sounds, mostly according to context. And to make matters more complex, they may even be completely silent, such as the "K" in the word "know" or the "E" in "late". The sounds corresponding to "know" and "now", would just be written as "nou" and "nau" in Latin.
What is even more strange to someone native to a Latin-derived language, such as Spanish, is that English uses two written vowels to represent one spoken vowels (such as "eat"). Or conversely, use a single written vowel to represent two or more vowels (such as the "a" in "ate").
Latin has 5 vowels, but English has many more. In latin you have just one "A" sound, but its equivalent in English has three variations, as the sound in "cut", "cat" and "car" are not the same. Don't be surprised if someone native to Spain uses the same vowel for "cut", "cat" and "car". Many non-natives find it challengeing to distinguish these sounds which just seem too similar to them.
With that being said, the question is why then, spelling and pronounciation is so notoriously hard to learn in English. The answer is that the Latin alphabet was not invented for it. The Latin alphabet was spread all over Europe during the second millennium, and English eventually was forced to adopt it.
Throughout history there have been several attempts to make English spelling irreducibly simple, so that each letter corresponds always and only to a single sound. In the last century, John R. Malone designed an alphabet called "Unifon". Logically, it had 40 characters, each corresponding to one of the 40 phonemes that make English speech.

However, as the alphabet reused many characters already present in the Latin alphabet, some people noted that it would be confusing for English speakers to learn it, as they are way too used to pronounce those characters according to context. Old habits die hard, and it is the same for pronounciation.
Some ten years later, the Shavian alphabet was invented.

Like Unifon, it also had 40 characters with each corresponding to only one phoneme. However, it was better in many ways. First, the symbols themselves look completely unlike Latin characters, in order to avoid having the previous "relearning" problem. Second, letters that represent similar sounds are just flipped or rotated versions of a single symbol, so that it is more intuitive. Thirdly, there were unique characters representing very common words such as "to" and "and". Finally, writing in Shavian is quick, as all characters can be written with a single hand movement.
It was very simple... But did not get popular after all, because yet again, old habits die hard.

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Why White Blood Cells (WBCs) do not react to foreign bodies like sperm?
Why do the white blood cells allow foreign bodies like sperm to exist inside body cavity without any reaction?
White blood cells function is to fight against foreign bodies (from the text books).

Majority of white blood cells in general are present only within blood vessels, lymph vessels and lymph nodes. In addition various organs have locally adapted specialised immune cells. For example brain has microglia, Liver has kupfer cells, etc... Specialised immune cells are present along the mucosal linings which are named differently in different regions - Peyer's patch in the jejunum and ileum, tonsils in oral cavity, adenoids in the nasopharynx, etc...
As sperm do not enter blood vessels, only local mucosal immunity will act on them. There is a local immune response to the sperm in the vaginal mucosa. However, the immune response to the sperm is transient. Several hypotheses have been put forth to explain this:

The seminal plasma suppresses the immune response. This is supported by the fact that sperm, if introduced without seminal plasma, do elicit an immune response--however this suppression seems to be inconsistent
Insemination might activate a sequence that results in active immune tolerance to paternal antigens (antigens present in sperm)

For details see here:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782486/

Studies show semen does mount a considerable immune response in the female mucosa, however:

Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


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How long do zebra fishes remain transparent?
As larva, zebra fishes are transparent, at least up to 5-6 days. I wonder what would be the upper limit of the transparent period. This is of relevance considering purposes for imaging.
The question primarily relates to normal zebra fish, and not especially to transgenic breeds.

I slightly re-worded your question for clarity. Feel free to roll back.

The upper limit of transparency time of zebrafishes is anywhere from two to three weeks for normal zebrafish for optimal high-resolution imaging. However, there is a modified species of Zebrafish called 'Casper' which is now the preferred zebrafish strain for studies in cancer and other research, because the length of transparency lasts into adulthood.
Sources:

http://medicalphysicsweb.org/cws/article/research/51394
https://biology.mit.edu/people/lisa_steiner#research_summary
http://www.the-scientist.com/?articles.view/articleNo/34834/title/Models-of-Transparency/


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Are alleles passed down and shuffled randomly to the offspring during meiosis or fertilization?
If it does occur during meiosis, are the alleles switched over from one sister chromatid to the other during the crossing over process in Prophase I?

Crossing over/synapsis in Prophase I of Meiosis I is when alleles are switched over from one non-sister homologous chromatid to another non-sister homologous chromatid. This happens before fertilization ever happens. Meiosis occurs even before birth in females in order to make gametes in the form of oocytes. In contrast, this frequently occurs in men who continue to produce gametes in the form of spermatocytes throughout their lifetime. Fertilization simply refers to the fusion of two gametes-- a spermatocyte and oocyte combining together-- and does not involve meiosis.
Here's a short and straightforward Youtube video about Meiosis.

Crossing over generally involves homologous chromosomes.

Meant to say "non-sister". I'll make the correction. Thanks!


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Why do reptiles still move even after death?
I saw a video in which a decapitated snake head still tried to bite.
I also saw a video in which a man was hit by the moving tail of a dead crocodile.
So why do reptiles move even after death?
http://en.wikipedia.org/wiki/Reptile

I think it is not only reptiles - chicken are notorious for dong this, and insects as well: http://biology.stackexchange.com/questions/23842/why-does-a-cockroach-not-die-even-after-decapitation?s=1|1.0349

Perhaps the problem here is with your definition of death?  Death is not (usually) an instantaneous state change, but a gradual process. The decapitated snake or chicken is dying, but not yet dead.

In warm-blooded animals, our high metabolisms are a significant disadvantage when being decapitated. Just a few minutes without oxygen and a mammal's brain is caput—the result of a massive cascading cellular die-off. Not so with cold-blooded reptiles. Their slow metabolism sustains their internal organs for far longer than a mammals causing them to completely die far more slowly. Essentially, cutting off their heads only makes them "mostly dead".

Can you add some references to your answer?

Reptiles stimulate impulses after death due to reasons, lets see snake for example.
Snake after been crushed still moves because of the electrically charged ion in the nerve calls of snake, as the brain continuously send messages through the nerve cells, note that the brain of snake need the least amount of oxygen for survival so does not die as quick as you may think, the brain can still live for about 1hr after the body of the snake stopped stimulating impulses.
Be advised, never put your finger in a Dead snake's mouth as it can still harm.

Welcome to the forum. It's good practice to provide reference for your claims (such as books or scientific publication or at least web pages).


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Can canines communicate with each other using gaze direction?
After researching why humans have white scleras when most primates have dark scleras, I stumbled upon the cooperative eye hypothesis. It proposed that white scleras may have evolved on behalf that it is an effective form of communication in that it makes the iris stand out and enables another to clearly see where the eye is looking so as to read expressions.
I noticed that dogs, which also have white scleras, use eye direction periodically for expression. Does the cooperative eye hypothesis apply to canines as well? If not, then for what reason might dogs utilize eye movement as they seem to do? Might such a thing be learned behavior?

It is hypothesized that the starkness of white sclera against darker colors of the pupil and iris is a unique mutation in primates that have become prevalent in human beings because it enhanced our ability to communicate with other humans and animals, including dogs, by more clearly communicating where we are looking.

However, it has not yet been established that dogs use this communication with each other, communicating more commonly with other means such as body language, head direction, vocalizations, etc. Some dogs, especially domesticated ones, do have white sclera and it is proposed that this is due to unintentional selection by humans who have a preference for such features.

What is extremely fascinating is that this 'mutation' occasionally occurs in chimpanzees and apes, too, but has not become prevalent in their respective populations.

Sources:

Secret Life of Dogs- BBC Film
Do the Eye Have It?-Academia
Common feature in domesticated dogs-CARTA
Juvenile features-NIH

"it has been observed that dogs do not use this as communication with each other" I saw no evidence of this in your cited papers. Can you provide support for this claim? That is, after all, the OP's question.

His original question asked if the cooperative eye hypothesis applied to canines.

I'll clarify what I meant to say.

A new study published in the journal PLoS One compared facial characteristics, gazing behaviors, and sociality of 26 different canid species (including wolves, bush dogs, and Arctic foxes). The researchers found that animals with eyes and facial features that are easier to discern are more likely to live and hunt socially. (One of the authors, S. Kohshima, has studied the morphology of the human eye, its adaptive meaning, and has done comparative studies on external morphology of the primate eye.)
In this paper, the authors identified three face-eye types based on four contrast indices: the A-type, in which both pupil position in the eye outline and eye position in the face were conspicuous (11 species, including wolves and coyotes); the B-type, in which only eye position on the face was conspicuous (9 species, including the Fennec fox and jackals); and the C-type, in which both the pupil and eye position were inconspicuous (6 species, including the bush dog and the African wild dog).

They compared group living vs. solo/pair living, group hunting vs. solo hunting, gaze duration and other parameters. Citing supporting evidence from other authors as well, they found that in species engaging in group living, 8 of 10 study species exhibit A-type faces. African wild dogs (C-type) use their white-tipped tails as visual signals, and like dingos, use vocalization, suggesting a developed acoustic communication. In contrast, gray wolves made almost no sound even during play or fighting but had more gazing behavior in more postures. Therefore, species with B- or C-type faces that in engage group living may use acoustic and/or other visual signals instead of the gaze signal as their primary means of communication (as is true for wolves and dogs). The enhanced gaze-signal of the A-type face could be disadvantageous during hunting, as prey animals could use the gaze signal to realize that they have been targeted by the predator and then prepare to escape. A-type faces were more common, then, in group hunting, where solo hunters were more commonly B or C-type faces.
In gray wolves, the gazing behavior (0.5s on average to humans, 3.32s average with up to 38s maximum with other wolves), termed conspecific with others of the same species, suggest that the gaze signal of gray wolves is mainly used for communication among conspecifics.

These results suggest that the facial color pattern of canid species is related to their gaze communication and that canids with A-type faces, especially gray wolves, use the gaze signal in conspecific communication... Our comparison of face morphology and gazing behavior among canid species highlighted the gaze-signal communication in species with A-type faces, especially gray wolves, and provided a novel perspective for studies on their communication and morphology.
Could the cooperative eye hypothesis apply to dogs as well? If not, then for what reason might dogs utilize eye movement as they seem to do?

Yes. (By the way, many dogs have white sclera.) The difficulty is that dogs are usually raised alone with humans and can lose the ability to "read" other dogs. One study, however, examined the behavior of dogs with human social cues (such as gazing) and conspecific (other dog) social cues. (Primates have been found to respond to conspecific social cues more than human gaze/pointing.) When the informant in this study (the one giving the cues) was an unfamiliar human, dogs responded well to gaze and gaze/pointing. However, when the informant was an unfamiliar dog (tethered, standing still, no human around to look at), the dogs were also able to follow the gaze of the informant dog, even when the body pointed elsewhere. Furthermore,

This skill with conspecifics is somewhat surprising because many of these domestic dogs had had only limited experience with other dogs. Indeed, the one intriguing developmental finding was that the 6-month old juvenile was only able to use cues produced by conspecifics, whereas two 4-year olds (the oldest in the sample) were only able to use human cues. ...it does suggest the hypothesis that many dogs are able to use conspecific gaze cues from early in life without extensive experience with conspecifics, and then ontogenetically, they extend this ability to humans (to some degree on the basis of similarities in human and dog facial features) as they interact with them - perhaps in some cases to the point that they lose their ability with conspecifics.

If more studies focused on conspcific cues among dogs instead of focusing on their interactions with humans, I think this behavior would be borne out and would be readily established.
A Comparison of Facial Color Pattern and Gazing Behavior in Canid Species Suggests Gaze Communication in Gray Wolves (Canis lupus)
Development of Gaze Following Abilities in Wolves (Canis Lupus) (interesting video)
Domestic Dogs (Canis familiaris) Use Human and Conspecific Social Cues to Locate Hidden Food
A Review of Domestic Dogs' (Canis Familiaris) Human-Like Behaviors: Or Why Behavior Analysts Should Stop Worrying and Love Their Dogs (just a cool paper)


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Why don't breast enlargements leave any marks of surgery on breasts?
If we get stitches, we get marks left on the skin, but there are no marks for breast enlargements. I saw a YouTube video about a breast enlargement wherein a doctor makes a cut. Where does the cut mark go after surgery?

All cuts that go through the dermis (the full thickness of skin) will leave a scar, no matter what (and no matter what anyone tells you). The visibility of scar tissue has a lot to do with how a person heals, how much stress is put on the incision as it's healing, where the scar is, if it crosses the natural direction of skin (called Langer's lines) or goes along the lines.
Plastic surgeons have many years of training and experience in cosmetic skin surgery, and know how to minimize scar formation by their more fastidious closure methods and wound care, as well as hiding scars in ceases and along Langer's lines. But even the best plastic surgeons cannot prevent scars, only minimize them. If you still don't believe breast augmentation doesn't leave scars, you can look at this page (NSFW).

They don't always cut through the breast.  The armpit is a common alternative to slicing the breast tissue.  In these cases, there is absolutely no scarring on the breast of any kind.


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Plasmid in the nucleus and gene expression
If we insert a plasmid into a human nucleus that contains exact copy of gene and all relevant promoters to produce some human protein,  will the cell create functional protein from that plasmid only when the cell needs it?
I am not talking about inserting DNA to some chromosome. Inserting separate plasmid to the nucleus (transient transfection).

If you transfect cells with plasmid then these plasmids need to go into the nucleus (otherwise they wouldn't be transcribed). Getting the plasmid either happens during cell division (when the nucleus is not present) or by adding a signal sequence to the plasmid which induces the import into the nucleus through nuclear pores. The SV40 sequence is an example of such a sequence.
If you have the right promoter present on the plasmid, you can basically express any protein in the cell (unless it's toxic). The promoter either needs to come from the organism from which the cells are or has to be something universally activated like the CMV promoter (from the cytomegalo virus).
A good example for this is the expression of green fluorescent protein (GFP) which originates from jellyfish and can be expressed in cells to make them glow green (from here):

Untransfected cells or cells transfected with an empty plasmid (without GFP) don't glow.
Targeting specific cells or control the specific activation of genes only in one cell type is possible. For both you need sequence (and cell specific) promoter sequences which either allow the nuclear import (see reference 1-3) or the expression from a cell type specific promoter (see reference 4).
This has been done in the liver of mice in which the ApoE has been knocked-out. The expression of the human ApoE gene with a specific promoter led to the correction of the hypercholesterolemia the mice were suffering from. This needs a lot of knowledge on the promoter as well as on the other transcriptional regulation elements in the specific gene (see reference 4).
References:

Cell-specific nuclear import of plasmid DNA.
Tissue-specific and transcription factor-mediated nuclear entry of
DNA.
Progress and prospects: nuclear import of nonviral vectors.
Sustained liver-specific transgene expression from the albumin
promoter in mice following hydrodynamic plasmid DNA delivery.

Thank you, Chris. I edited the question, it may be not clear, I mean some human protein, that existing in normal human cells. Lets say - the DNA that code for that protein is damaged and now we inserting plasmid with working one. So will the cell create now working protein too, and only when the cell need it? Thank you again.

That's harder, I will edit the answer.

@chris GFP comes from Quail? I thought it came from a jelly fish. And nuclear entry isn't easy, plasmids don't just enter the nucleus. In rapidly dividing cells, they can enter when the nucleus breaks down during mitosis. Getting them to move through the nuclear pore complex is tougher.

@user137 You are right, I used the wrong word. Also about the entering of the nucleus. I edited the posting, thanks for the correction.

@Chris The SV40 sequence is an interesting one. David Dean has done a lot of work on cytoplasmic transcription factors binding to plasmid and pulling it into the nucleus. My boss doesn't believe it, I'm undecided. Quite a few papers about it, but I haven't tried any experiments myself. I suspect the transfection agent used can alter how well it works, because if your PEI or lipofectamine or whatever doesn't dissociate, the transcription factors might not be able to reach their binding sites.

@user137 Interesting thought. It might then also be possible that the transfection reagent helps going through the nuclear membrane as well.


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Is there anything that is completely non-toxic to humans at any dose?
Lately I have seen a number of unrelated "scientific" debates over whether certain substances should be outlawed because they are toxic to humans. My initial, informal reaction is usually to respond that anything is toxic to humans if you give them a sufficiently large dose.
However, formally I don't know if that's really true for everything a human being could ingest in some way. I started to wonder if there were some substances that our body could handle unlimited amounts of without any negative consequences.
As this question has been (correctly) identified as a bit vague, I'll try to explain what i'm looking for. For the purposes of this question, I'm willing to ignore the limitations of actually ingesting a given substance in "the usual way". For example, if you can't physically drink enough of some liquid fast enough to kill you without your stomach filling up and vomiting, but that same liquid injected intravenously could be lethal, I could consider that toxic. I also recognize that the body can only physically contain a certain volume of stuff, after which sheer pressure would cause it to fail; I'm more interested in "biochemical toxicity" as opposed to any physical damage (I just don't know the term for what I'm looking for.)
In other words, one of my goals is to learn if, under laboratory conditions, a properly motivated researcher could always find a dose that would be toxic, regardless of the impracticality of a real person ingesting that dose under normal circumstances.
So, with that qualification, my ultimate question is:
Is there any substance we know of that is completely non-toxic to humans at arbitrarily large doses ingested over an arbitrarily short period of time?

Strictly speaking, I suppose the inert gasses (Helium, Neon, Argon, &c) wouldn't be toxic.  Likewise metals like gold & platinum that have low reactivity.  Though swallowing a bunch would probably kill you by mechanical obstruction of the digestive tract.  More interesting to me are things like vitamin A, which are necessary for health at small doses, but toxic at larger ones.

I rather think there's a lot of things that would kill you at a high enough dose, but I don't think qualify as toxic.  Like matching blood plasma clearly won't be toxic, but eventually the increased pressure would kill you.  Can you clarify your question as per this?

@MooingDuck I hope that helps. I just don't know the word that means what I want; i want "toxic because it interacts biochemically with the body, not because your kidneys rupture under the pressure."

@jamesqf: Gold actually is toxic at high doses. According to https://www.rarediseases.org/rare-disease-information/rare-diseases/byID/669/printFullReport, "Overexposure to gold (as in treatment of rheumatoid arthritis) may cause skin rashes; bone marrow depression; stomach and intestinal bleeding; headaches; vomiting; focal or generalized continuous fine vibrating muscle movements (myokymia); and yellowing of the skin, mucous membranes, and whites of the eyes (jaundice)." (The same page also mentions platinum poisoning, but gives no information about it.)

@ruakh: I think that refers to poisoning by various gold compounds, not from elemental gold.  Compounds are of course not the same as the elements of which they're composed, otherwise a few grains of salt would kill us.

@jamesqf: Hmm. But gold poisoning is a kind of heavy metal poisoning, and is susceptible to the same type of chemical therapy (namely chelation) as other kinds of heavy metal poisoning. And -- as you say -- there are "various gold compounds", and all behave the same way. So the issue is presumably gold ions? I have no idea whether dissolved gold atoms could undergo some sort of redox reaction and become ionized during the digestive process, or as they go through the bloodstream.

@jamesqf, not all inert gases are non-toxic. Xenon is used as an anaesthetic. Too much of it and you suffocate, not because it displaces oxygen, but because it inhibits breathing.

@ruakh: That's something I've always been vaguely puzzled about.  Seems to me (though I'm far from an expert) that heavy metal poisoning isn't from the metals themselves, but from various compounds/ions.  So if the metal is fairly non-reactive (like gold) you could swallow chunks of it and be unaffected.  Or for instance all the people with gold or almagam dental fillings, or other implants.

@jamesqf Yeah, heavy metals have their toxic effects in some ionized state, in which they substitute for a lighter metal that's used as a cofactor on some critical metabolic enzyme, causing it to malfunction.  If you swallow a lump of the un-ionized metal, it'll be basically a question of how much your digestive system can corrode it, which for gold = hardly at all.

Silicones are pretty inert substances but finely divided silicone (dimethicone) will have laxative action and unlimited consumption can be harmful.

I’ll answer this theoretically, since that’s how it has been posed. And if we’re ignoring practicalities, we may as well posit that the substance in question will be introduced directly into the bloodstream (This is, of course, simple to do in reality, but not how most people consume their non-toxic substances.) The easiest way to show that any unspecified substance can be toxic at an unlimited volume is to invoke the human body’s mechanisms for volume homeostasis.
As mentioned in this answer, the human kidneys functioning optimally can produce up to ~ 25 L/day of urine.1 This would require complete suppression of ADH (anti-diuretic hormone, a.k.a. arginine vasopressin), which would occur only if the “toxin” load were markedly hypotonic (think water).2  There is therefore a theoretical maximum volume of any substance that can be dealt with by the body, which is something less than 25 L per day. (For any substance other than water, the maximum will be lower because ADH will not be as fully suppressed by a less hypotonic load.)
A volume of any substance introduced into the bloodstream (including a product precisely mimicking the constituents of the bloodstream itself!) will overwhelm the body’s homeostatic mechanism. This will result in edema which is unpleasant and, in the case of pulmonary edema, certainly pathologic - a “toxidrome” in your scenario. In the case of hypotonic fluids, serum osmolality will also fall causing hyponatremia with all of its consequences.
Summary: No, the human body can not tolerate an unlimited volume of anything, therefore there is no substance that is non-toxic "at any dose."

1. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.

2. No, you may not drink 25 liters of water per day. For one thing, urine can not be made with a tonicity of 0 to balance this (more like 60 mOsm/kg minimum). Additionally, ADH can rarely be completely suppressed, yielding a somewhat more concentrated urine and therefore lower tolerance for hypotonic intake before serum osmolality is compromised.

"the human body can not tolerate an unlimited volume of anything" - This is basically a tautology.  It doesn't even matter how the kidneys work - no matter how the human body works, there is no way it could tolerate of unlimited volume of something.  Even a never-ending hole in the ground will overflow if you pour fast enough, no matter how big it is.

@BlueRaja-DannyPflughoeft - The question posited "an unlimited amount," not me. :-) This just seemed to me the easiest route to address a question that is otherwise difficult logically (to "prove" that no such thing exists). I went through the factors that dictate that physiologic limit for volume intake and the toxicity of exceeding it, which is why I considered it substantive enough to be an answer. You may disagree.

I know, I upvoted your answer.  I just think it's a silly question.

Not a silly question at all, though perhaps needs to be re-worded to add qualifications about amounts a person could potentially consume - as for instance water being toxic in large amounts.

This answer does get effectively what I was looking for, though I've tried to reword it to be more clear about what I meant by "arbitrarily large". Hopefully that helped?

@MichaelEdenfield The question is pretty highly upvoted, so I wouldn't worry too much. :-) Your edit did clarify your intentions. I actually think I've undermined them a bit by making it about volume rather than dose in any normal sense of the term. But if you want talk about the "most benign" sorts of infusions, my mind goes to isotonic saline or some (hypothetically non-immunogenic) whole blood product, and then the limiting factor is obviously volume. Anyway, glad it was helpful.

@Susan yes, I unaccepted your answer since I've clarified the question a bit and it doesn't really fit the clarified question. I still think this answer gets closest to what I was looking for, especially the information about the kidney's limitations on how much work they can really do, but I want to give other a chance to chime in before I re-accept it.

The kidneys don't always have to get rid of all the water a person drinks. In some circumstances a lot of water can be excreted through the skin and lungs.

@bdsl Yes, good point, I had considered mentioning these insensible losses, but the volume is relatively small in healthy individuals compared to what we're talking about here, and to my knowledge they aren't regulated (like the kidneys) in a way that allows them to participate in the dynamics of volume homeostasis (i.e. they are fixed or environmentally dependent rather than responsive to volume/solute load).

There is an applicable norwegian proverb that says; "Health in every drop, poison in every liter".

It depends largely on the method of administration. If you are atomizing the substance and delivering it via water vapor, many, many substances have no known LDLo (lowest dose required to kill a member of the tested population). Almost any substance in existence has the potential to kill you if it is diluting your bloodstream via direct intravenous injection or oral consumption; however, when it comes to inhalants, many substances cannot kill you.
Since your question was specific to intoxicants, here's a couple of examples: There is no LDLo level of Tetrahydrocannabinol (the active ingredient in marijuana) when delivered via atomization. There is also no known LD50 (a similar, albeit somewhat less reliable, metric) for lysergic acid diethylamide (commonly referred to as LSD). For psilocybin (the active ingredient in "magic mushrooms"), the LD50 is high enough that an average person would need to ingest around 6 pounds before cause for concern.
Other far more dangerous substances that can kill with vastly lower amounts include anything that speeds or slows the heart rate: most specifically, cocaine (including crack), opiates (including morphine, heroin, and various pain pills), and any amphetamine, methamphetamine or derivative substance, or other stimulant (crystal meth, ADHD medication, and even caffeine or ephedrine). Of course, the most common killer categorically from a historical perspective is alcohol.

to be honest, I was motivated by the claim that propylene glycol (what's in most e-cig liquid) was toxic. But I also know that at least one THC study claimed that THC was toxic after IV-injecting it into rats at thousands of times a normal dose, which motivated the exact wording of my question.

The absence of a known LD50 doesn't mean there isn't one.  It just means it's beyond what anyone has been exposed to.

Poor rats... :(

There is a problem with definition of toxicity — things that are dangerous in large amounts aren't usually called toxic. In spite of this, you're right: everything can be dangerous to a human in large enough amounts, or if delivered improperly.
For example, even water can be toxic if drank too much. Also, when it gets into the lungs, it may cause drowning.
On the other hand, air, while necessary in lungs, is dangerous if present as a gas in the bloodstream.
BTW, even botox (being one of the strongest poisons) is used in medicine in very small doses.

True, I knew the word toxic was being used sloppily, but that's the word I see used to describe things like IV-delivery of absurd amounts of THC, so I didn't know what other word to use.

First thing I thought of when I read this... and I remember reading about this way back when w/r Water Intoxication: http://www.cbsnews.com/news/woman-dies-after-water-drinking-contest/

The inert gasses Helium and Neon are non-toxic when administered through inhalation, so long as the patient's oxygen supply is sufficient.  They are also non-toxic when injected, so long as the injection is slow enough for them to be dissolved in the bloodstream.
You can be killed by them through various means (asphyxiation through oxygen displacement, rapid injection causing an air embolism, rapid decompression causing decompression sickness, and so on), but since the cause of death is unrelated to the chemical properties of the substance involved, it's not accurate to call this "toxicity" (unless you're XKCD).
Other inert gasses (Argon, Krypton, Xenon) may be toxic at high pressures: although I haven't found an LD50 for any of them, they can all induce nitrogen narcosis, and Xenon is usable as a general anesthetic.

Wrong.  All the "inert" gasses will kill in sufficient quantity.  It requires considerably more than you can breathe at normal atmospheric pressure but if you run the pressure high enough they turn evil.  This is what imposes the limit on scuba diving--there's no gas mixture that doesn't become toxic at a high enough pressure.

He, he :) Indeed this question smells like XKCD - arbitrarly large numbers are quite often in What if :)

@Loren Pechtel: But is it the toxic effects of the gas itself, or just that it's something saturating the blood at high pressure, then coming out when the pressure is reduced - that is, 'the bends'?  Maybe splitting hairs, but I see it as like the difference between the toxic effects of drinking too much water, and drowning.

@LorenPechtel, I've updated my answer to take into account nitrogen narcosis, since Ar, Kr, and Xe can induce it.

@Mark I doubt anyone knows the LD50 for them.  Where would the data come from?  They're going to stop using them at the depth where the symptoms become serious, nobody's going to take them to a lethal depth.  And it's not just Ar, Kr and Xe, H and He also do it.

@jamesqf No, I'm not talking about the bends, but rather what's more commonly known as nitrogen narcosis.  Everything we can breathe (except oxygen, which has it's own problems in excess) will cause it if the pressure is high enough.

@LorenPechtel, the usual way to find an LD50 is to kill off a bunch of lab rats.  For something exotic like high-pressure Argon poisoning, it's probably not worth the effort.

@Mark Yeah, you could get a LD50 for rats that way but why bother?  It's not something that's a realistic threat to a human--you'll kill yourself by accident before you get that deep.

not even AIR, because if you force too much you will explode it depends on how extreme is the "any dose" statement
water is also toxic in large Ingestible amounts
and since we go into theoretical application the answer would be dark matter
so the final answer is nothing , because the human body has evolved to exist in some equilibrium, so too much of one thing even if is harmless it itself ( like water, or proteins ) it causes an imbalance, and as a result it becomes "toxic"

Even simple water is "toxic in high amounts" as kidneys can remove 25 l per day at most. All other substances are probably even more "toxic".

Downvoter, please leave a comment.

Vitamin C won't kill you no matter how much you get into your body as long as it is enough to help prevent arterial wounds and atherosclerosis(This happens in people with scurvy or vitamin C deficiency because of how cholesterol is used to help repair the wounds and this can lead to a complete blockage of the artery and thus an infarction of all the tissue that artery supplies. So if you don't want to have an MI, one of the things you have to do is get vitamin C into your system.
Another example of this is chloride ions. While having high chloride ions might cause there to be a slower reaction time(since chloride acts as an inhibitor in neurons) it itself won't kill you. Yes it might affect the muscles by not having them contract as much as they are supposed to but this is naturally cured by urinating out more chloride and thus more sodium which can lead to a sodium deficiency which is bad because your body needs sodium in order to function. With a low amount of it it you wouldn't be able to think clearly or even have a normal heart rhythm which might lead to bradycardia from a higher pottasium concentration in the heart.

Doesn't your second paragraph just explain that chloride is in fact toxic at some dose? (The MI/high-dose vitamin C association also needs some referencing, except it's not really relevant.)

Wikipedia indicates that it is unknown if vitamin C can be toxic or not.  It cites a source (at a dead link) that apparently managed to kill rats by administering excess vitamin C, but it is uncertain whether the cause of death was chemical or mechanical.

No. The second paragraph says that while chloride is nontoxic at a high dose, high chloride results in low sodium and it is the low sodium that is toxic. as far as the association of scurvy with MIs that is actually relatively simple. When somebody has scurvy this causes them to easily get arterial wounds both external and internal. The body uses cholesterol to heal these wounds in somebody with scurvy instead of platelets. This is turn causes more cholesterol to build up in the artery causing atherosclerosis. If this happens in the heart than it can cause a heart attack or MI.

And as far as the death from excess vitamin C it was probably mechanical and not from the vitamin C itself. And even if it was from the vitamin C that does not mean that excess vitamin C in humans will cause death. In fact I have been taught that since vitamin C is water soluble and vitamin C always helps your body by strengthening your immune system and acting as an antioxidant that vitamin C toxicity does not exist, only deficiency.

high chloride results in low sodium and it is the low sodium that is toxic : you’re describing a mechanism of toxicity there, not the absence of toxicity.

This is not really a substance, but anyway.
Neutrino
Neutrinos are ghostly particles that barely interact with any matter. Therefore, no sufficient amount of neutrino (that human can ever collect) can kill you. To have a lethal dose of neutrino radiation, you must stand inside the outer layout of a giant star that creates a supernova.
Source: XKCD, Lethal Neutrinos

The source you link (and your last sentence) say there can be a lethal dose of neutrinos. The point is just that it's hard to kill anybody with neutrinos because the usual sources of lethal doses of neutrinos also produce large amounts of more lethal particles, radiation and heat and therefore a human would die from other causes long before being exposed to the lethal dose of neutrinos. Therefore, neutrinos aren't an answer to the question.

I agree. It's just that so is the top voted answer. So I take my deliberation and post this answer


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Cannot conjugate Biotin-labeled DNA to Streptavidin-labeled solid surface
I have been trying to immobilize DNA by the bioconjugation of biotin and streptavidin, but I cannot get this work.
I added EDC and streptavidin to COOH functionalized resin, reacted for 3 hours in room temperature, and then washed with PBS.
Then I tried to anneal biotin-labeled primer and FAM-labeled complementary sequence. (Heated it up to 95 degree then let it cool down to room temperature.
After I added SA-functionalized resin and FAM-Biotin strands together, the conjugation wouldn't work. The resins are not fluorescent after wash.
I also tried to use PCR products which are labeled on both side.
Is there any problem with my assay? How long it takes for the conjugation of biotin and SA at very low concentration?
Thank you for any information.

Are you certain the resin has streptavidin? Can you get some biotinylated fluorescein or other dye just to check the streptavidin? HABA dye might also be helpful to determine if streptavidin is bound.

@user137 Thank you for your advice! I am not sure if resin is successfully functionalized, as I don't have any dye to check for now. Maybe I should purchase one for this. I don't see any reason that SA is not bond, I saw a lot of paper use this method.


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SNPs and locations
I am new to reading raw DNA. When comparing two people's raw data, why does one person have a different SNP than the other, at the same location, on specific chromosome? But on a different chromosome there will be the same SNP, at the same location, for both people.

Genetic variation, my friend. People are bound to share similarities and have differences in their DNA, as influenced by errors in transcription, the environment, inheritance, etc. SNPs can be functionally significant or insignificant.

I think it is important to point out that "on a different chromosome [..] at the same location" is not the same location, and that there is not necessarily any relation between similar positions on different chromosomes. I presume you mean something like 'at basepair #74 501 on Chr1 and then also basepair #74 501 on Chr6'. These are totally unrelated positions in the genome, these chromosomes are independent. 2 genomes may vary at one position and not at the other, it's unsurprising.
Is this what you mean? We should be clear about this.

Because that's how genetic variation works. SNPs are called single nucleotide polymorphisms for a reason: they are polymorphisms. This means that they are loci where different individuals will have a different nucleotide. This is precisely why they are studied and why we have databases of SNPs and the various genotypes they can manifest.
Remember that mutations can occur spontaneously in a single individual. In fact, they can appear spontaneously in a single cell. This means that if you sequence the genome of two different cells of the same individual it is actually possible that you will find small differences.
Finding small differences between different individuals is certain. Our genomes are not identical and while most differences will be in non-coding regions, you will also have SNPs within genes. How much of our phenotypic variation depends on such small differences is an active topic of research but it is safe to assume that small, single nucleotide changes cause at least some of the variation you see in the people around you.
In any case, what would be surprising is if two individuals were to share the exact same SNP forms for all SNPs in their genomes (I'm sure this happens, but I would expect it to be the case only for close relatives and probably not even then). This variation is the whole point of SNP and the only reason we analyze them.

It sounds to me as though you have misunderstood something about the chromosomes that make up a human genome.

on a different chromosome [..] at the same location

is not the same location at all. There is no surprise in finding 2 genomes to differ in one place, and not at another unrelated place.
edit If this is a mis-reading of your question, and you meant that the 2 persons' SNP was "at the same location" as the other person, then the rest of the answer is irrelevant. 'A SNP' refers to a location, given a name/identifier for the purpose of measuring variation with SNP-chips; necessarily the same location in any person, which may vary, but needn't always differ between everyone (come on, there are only 4 possible values). You should re-phrase your question "why do they differ at SNP 1 and not at SNP2?".
Background
SNP means nothing more than 'a single basepair in the genome, that might vary in a population', so let's just talk of 'difference at a position'.
A single haploid set of the human genome consists of 23 chromosomes, 22 of these are quite 'ordinary', while 1 is involved in sex determination. Of course, most of our cells are diploid and so we have 2 of these sets, with pairs of Chr1, Chr2, ...Chr22 and X/Y.
What I think your problem isn't, that you perhaps thought it was
I haven't analysed large bits of genomic data but I believe heterozygous positions (positions at which one individual's paired chromosomes differ) are represented in that individual's sequence data. For this reason, I do not think your question is asking 'how can 2 persons have a difference at basepair x on one copy of Chr1, and no difference on the other copy of Chr1' - because both copies of Chr1 are merged as one person's dataset.
In fact it's impossible to assign (meaning to group in to haplotypes) heterozygous sequence to either one copy or the other without more information, i.e. sequences from parents & grandparents, to see which variants are inherited together (are linked).
What I think your problem really is
I think you are asking 'how can 2 persons have a difference at basepair x on Chr1, and no difference at basepair x on Chr6 (say)?'
This is easily answered. Basepair 100 of Chr1 is a completely different and unrelated position in the genome to basepair 100 of Chr6. There is no reason to expect that these positions should be related.
A helpful thought experiment
We can concatenate the chromosomes rather than re-setting our count at the beginning of each, then bp 100 of Chr6 will instead be denoted (approximately) bp 1,080,000,100 of the genome - this makes the difference in these positions crystal clear.


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Why not use lactase to aid the break down of lactose when making biofuels?
I did an experiment using nine different substrates (Lactose + lactase, corn, sugar cane, glucose control, wood, grass, no yeast control and yeast control) and observed their fermentation rates. Lactose + lactase had the highest fermentation rate. So now my question is: is there a usage of lactase in aiding the break down of lactose to make biofuels? I did a web search and all I could find was that lactase was used for helping lactose-intolerant people,etc.  And that the current whey-ethanol industry used special species of yeast that break down lactose directly instead of the enzyme lactase. There are other methods too, including the Carbery and the Bio-process Innovation (BPI) processes; all of which use yeast that can directly break down lactose. Does lactase play no role in the biofuel industry? And why don't people use lactase to aid them in making biofuels?

Lactase on its own doesn't ferment anything. Also, yeast produce lactase in response to lactose.

Cost, I imagine. Lactase is probably harvested from yeast exposed to lactose, so it seems a little odd to grow the yeast on lactose, harvest the lactase, then put that in a mixture with other lactose. Skip the middleman and put in the yeast directly, plus then it replicates.

I agree with you Resonating. I think adding extra lactase enzyme would be an extra step. And would be expensive...


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Thermodynamics of Forming Peptide Bonds

Which of the following shows the correct changes in thermodynamic properties for a chemical reaction in which amino acids are linked to form a protein?
A) +ΔH, +ΔS, +ΔG
B) +ΔH, -ΔS, -ΔG
C) +ΔH, -ΔS, +ΔG
D) -ΔH, -ΔS, +ΔG
E) -ΔH, +ΔS, +ΔG
Answer:  C

I know that dehydration is endergonic (+ΔG).
I have two questions:

Why is entropy decreasing? In the beginning of the reaction, we have two amino acids. By dehydration, we have at the end two molecules: the two amino acids together and the H2O molecule. The same number of particles before and after.

Why is enthalpy change positive? You made a bond between the two amino acids. That is exothermic.

I don't think C is the answer. Answer should be D. There is a net lowering of enthalpy because it takes energy to break a peptide bond.

The energy used to catalyze the peptidyl transferase reaction is from the breakage of the bond between the amino acid in question, and the aminoacyl-tRNA it's attached to. The two reactions are coupled by the ribosome. The ribosome can then lower the entropy by positioning of the molecules (including water) in the active site as described here.
So we have our reaction ΔG = ΔH - TΔS
Your ΔG is positive because your reaction is endergonic, and the ΔH is positive because the peptide bond is the system, and you're absorbing energy to form it. The entropy is decreasing as such (removing enerygy = removing heat from outside the system), and the actual reaction for the formation of a peptide bond is unfavorable. As I mention above, this unfavorable reaction is coupled to a favorable reaction in the hydrolysis of an aminoacyl-tRNA to make it possible. What I forgot to mention above is that the ribosome is making this more favorable as well by decreasing the activation entropy for the reaction, and that's what they describe in the linked journal.

Please answer both questions to make the answer complete.

@yolo made what i thought were sensible edits.


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Why sperm count matter for pregnancy?
In order for a woman to become pregnant, sperm is needed. Why is sperm count so important for pregnancy?
http://en.wikipedia.org/wiki/Sperm

There are so many things that go into this issue: Sperm count
Ability of sperm to swim (motility)
Velocity or forward progression of the sperm
Size and shape of the sperm (morphology)
Total semen volume
The liquefaction of the semen (the ability to go from normal gel-like state at ejaculation to a liquid state)
Read more here

It's more than just sperm count that matters for a pregnancy if you are considering normal methods of insemination such as intercourse or assisted methods such as artificial/intrauterine insemination or in vitro fertilization. For couples having trouble getting pregnant, most OB-GYNs and/or Reproductive Endocrinologists/Infertility physicians do a semen analysis. This involves checking several things:

Ejaculate Volume (>1.5mL)
Sperm Concentration (>15million/mL)
Motility (>40%)
Morphology (>4%)

(and a host of other factors including rapid progressive motility, pH, etc). Why? Because there is no point of there being high numbers of sperm, if their motility is poor, because they won't be able to reach the oocyte. There's no point if they can reach an oocyte, if they are poorly shaped and cannot penetrate it. There's also no point in there being a high concentration of sperm, if the ejaculate volume is so low that it thins out before reaching the cervix. All these factors matter.
Total Motile Sperm Count (TMSC) is the most common way that physicians determine what route is best to increase chances for getting their patients pregnant.
TMSC = Concentration x Ejaculate Volume x % Motile (in decimals). Thus if, the value is:

greater than 10 million = normal male factor; check anatomy, check female causes
less than 10 million = low male factor; consider intrauterine insemination (IUI)
less than 5 million = severe male factor; consider in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI)

Sources:

Paper 1
Advanced Fertility

As sort of a generic textbook answer, there's a number of factors. The vagina tends to be acidic, much so it's within a range of intolerance for sperm. To counteract this, seminal fluid is often alkaline in nature (1). The cervix also tends to be covered in a mucus that sperm must penetrate to enter the uterus. On top of factors like sperm lifespan, tolerance to vaginal environment, etc. the necessary numbers to actually achieve fertilization is important.


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Why are sperm cells not attacked by the female immune system?
Whenever a foreign particle enters into someone's body, it is attacked by the white blood cells. I just want how it is that, when sperms enter the female body, they are not attacked by the the woman's immune system?

Studies show semen does mount a considerable immune response in the female mucosa, however:

Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


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How does Isoxaben kill newly germinating seeds, with almost no effects on established ones?
Isoxaben (N-[3-(1-ethyl-1-methylpropyl)-1,2-oxazol-5-yl]-2,6-dimethoxybenzamide) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

Here's the mode of action, as stated by Dow AgroSciences:

Isoxaben belongs to the Benzamide family of herbicides and inhibits cellulose biosynthesis in the cell walls of susceptible
  weeds (WSSA group 21). This means that cells cannot divide during the reproductive cycle; therefore, they cannot grow,
  causing death. While cell division does not occur, this mode of action should not be confused with mitotic inhibition that
  occurs with dinitroaniline herbicides.

How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?

As with your other question on mitotic inhibitors ("How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?"), inhibiting cellulose synthesis will inhibit growth. Hence, an established plant will stand its ground, but newly germinating plants cannot grow without cellulose synthesis and hence will fail to germinate.


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List of dinosaurs synonyms
Is there a comprehensive list of dinosaurs synonyms with indications of which name is now considered correct? Something like "there's no brontosaurus, there's only Apatosaurus", "there's no Anatotitan, there's only Edmontosaurus" and so on.

Here is one list that includes synonyms, but I don't know how credible it is and it seems to lack references. Encyklopedia of Life also includes information on synonyms (see link for Apatosaurus)- not a list but searchable.

Just for fun: This TED talk might be slightly related to your question.

Thank you Remi, this TED talk that i saw a few days ago is exactly what made me ask the question. I am creating a board game about dinosaurs and i need several names but i don't want to have two dinosaurs with different names that are actually the same dinosaurs and this is why i am here. I need a list, not a directory, just for convenience, because it would be so much more easier to scroll a list instead of looking for 120 different names (this is the current size of my dinosaur "pool"). thank you anyways!

@JohannesWentu For that use, the second list in my answer should be sufficient. It seems like several professional paleontologists are included in the project.

Actually, a paper in 2015 resurrected Brontosaurus as a valid genus. What is surprising is that the "thunder lizard" was smaller than the dully-named Apatosaurus.

Encyclopedia of Life includes information on synonyms (see link for Apatosaurus) - not a list but searchable and often with references and background info. After a quick google search I also found this list from dinosaurcentral.com, but I don't know how credible and updated it is and it seems to lack references.


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Heart Rate being normal when under treatment for the bends
When you surface from diving too quickly; you get "bends" - these are caused by gas bubbles forming in your lungs (especially nitrogen). This causes breathing problems if not treated since the bubbles are essentially blocking oxygen transport.
For treatment, you have to be in a hyperbaric chamber for several hours.
Why is it you don't get nitrogen and carbon dioxide bubbles in your bloodstream while being treated? I would think that in the machine the nitrogen, carbon dioxide and water concentrations would rise causing you to start having signs of low oxygen like loss of brain function.
As I stated previously, nitrogen bubbles block oxygen transport and thus carbon dioxide transport. Since there is nowhere else to go, it goes into the bloodstream where oxygenated blood is supposed to be. This is detected by the chemoreceptors in your arteries; this then tells the heart to beat faster in attempts to rid the body of CO2. Once again; however, this doesn't happen because now there are more nitrogen bubbles from breathing in more nitrogen and water. This leads to a progressively higher heart rate (Ventricular Tachycardia - V-tach) which is dangerous as it can lead to MI (Myocardial Infarction) symptoms - like chest pain. Ventricular tachycardia that lasts a maximum of a few minutes can then lead to V-fib (Ventricular Fibrillation) which, if not treated with epinephrine or defibrillation on time, will lead to asystole and death.

Summary:

When someone has the bends and is being treated in a hyperbaric chamber; how do they not end up having an acute MI (due to accumulation of nitrogen gas in the bloodstream)?

Can you please explain your abbreviations and also rephrase your question? At the moment it's hard to understand.

Does “a machine” refer to a hyperbaric oxygen chamber? I’m having trouble understanding the logic of the last sentence or what that has to with heart rate.

The point of "the machine" (hyperbaric chamber) is recompression, which stops the dissolved gases in the body to form bubbles in the blood. Then after treatment you can do a controlled decompression, similar to what you do during ascent in normal diving.

What makes you say there's no change in heart rate? Both the heart rate and the respiratory rate increase. But if you're talking about the effect of hyperbaric hyperoxia's effect on the parasympathetic nervous system, please clean up your question by editing it.

I ran some edits - hopefully you all will be able to understand the drift here :)

Allot of misconceptions regarding rapid decompression and the bends in this post; mostly none of what is mentioned happens unless the diver goes through extreme rapid decompression, and embolism is more likely to kill the diver in that case.  Recompression in a chamber re-dissolves the N2 bubbles and slow decompression prevents the return.

You have misunderstood bends, effects of high pressure on body and the need for recompression. If this question gets re-opened, it will receive great answers from a lot of people

You are wrong on several accounts:

Bends occur due to bubbles that form in muscles and joints and not lungs - They fall under Mild or Type 1 Decompression Sickness (Type 1 DCS).
Formation of bubbles in blood stream do occur in the Decompression process - Hyperbaric chamber is used to treat this condition.

What happens when diving:
During deep sea diving the pressure surrounding a person increases at the rate of 1 atm (atmospheric pressure) for every 10 m in sea water and 10.3 m in fresh water. This relation is linear.
The pressure inside the body equalises with the pressure outside to prevent any deformation. The solid and liquid components of the body can withstand pressures upto 151 atm (depth of 1.5 km underwater) without undergoing any noticeable compression. But air, being extremely compressible undergoes compression.
So at 2 atmospheric pressure the space occupied by the air in our body is halved. This would shrink the lungs to half the total volume. To circumvent this the divers breathe air compressed at the same pressure as the water pressure around them, so that the pressure gradient across the chest wall is normal.
Pressure Concentration relationship:

Dalton's Law:
This law states that the Barometric Pressure is the sum of the partial pressures of the individual gases in the air mixture.
Barometric Pressure - The total pressure measured

In air at 1 atmospheric pressure (760 mm Hg) the partial pressures of various gases are:

Nitrogen ~ 593 mm Hg
Oxygen   ~ 159 mm Hg
Co2 ~ 0.2 mm Hg
Others   ~ 7 mm Hg

According to this Law, as the pressure inside the Lungs increase, the partial pressures of each gas increases. At 2 atm, the partial pressures of every gas doubles.
The gas exchange in the lungs is based on partial pressure of the gases. Thus due to increased partial pressure, the amount of gases dissolved in blood increases (This increase is proportionate to the pressure levels).

During a extended dive (one lasting several hours) the body tissues gradually equilibriate with the high-pressure gases. At sea level our body contains 1 L of dissolved nitrogen, equally distributed between body's water and fat. As partial pressure of Nitrogen rises, the nitrogen equilibriates with the body's lipid stores because adipose tissue is relatively underperfused.

Once equilibrium is achieved the volume of nitrogen dissolved in tissues is proportional to the alveolar partial pressure of nitrogen. Thus at 4 atm the body will contain 4 L of nitrogen.
The same principle applies to oxygen as well, though the solubility of oxygen and the speed at which equilibrium is attained are different.
Decompression
During ascent from the depths, the Barometric Pressure (surrounding pressure Pb) falls. As the Pb falls the pressure inside the alveoli fall as well. This causes a fall in the partial pressures of all gases in the lungs creating a gradient of gases from the tissues to the alveoli.
So the diver has to ascend slowly to give enough time for the gases to move into blood from the tissues and then get washed out. If the ascent is too rapid, gases dissolved in the tissues - due to high pressure - attains the gaseous form (due to pressure drop) and become bubbles. This is similar to opening a pressurised coke can where one can observe gas bubbles forming.
The bubbles are the reason for the bends. Bubbles can also cause serious problems like arterial gas embolisation, CNS disorders (due to formation of bubbles in the myelin sheath of axons which compromise nerve conduction), pulmonary symptoms (due to pulmonary emboli), sometimes even Disseminated Intravascular Coagulation.
Solution
The decompression is done in stages - in which the divers spend various amount of time at various under water levels to allow complete diffusion of dissolved gases into blood and into the alveoli which is consequently breathed out.

Hyperbaric Chamber
The hyperbaric chamber is used when the above solution is not applied i.e. the diver has surfaced rapidly without spending sufficient time at various levels to allow proper decompression.
In a hyperbaric chamber the diver is recompressed to the pressures equal to the pressure experienced at the level to which the diver dived. Due to the increase in pressure, the bubbles get dissolved again. This instantly relieves many symptoms - like the nerve conduction delay, bends, niggles etc... Now the decompression is carried out by under controlled environment, simulating the various intervals the diver has to stay at various pressure levels under water.
Hope this explains your doubt.
So coming to myocardial infarction, the hyperbaric chamber redissolves the gas bubbles thus preventing myocardial infarction.

For more info read chapter 61 of Medical Physiology, 2nd edition, by Walter F. Boron and Emile L. Boulpaep.


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How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?
Trifluralin (2,6-Dinitro-N,N-dipropyl-4-(trifluoromethyl)aniline) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

From what I understand, the mode of action is as a mitotic inhibitor, which disrupts the microtubules that pull the cell apart when it divides (stops cell division).
How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?

Mitotic (cell division) inhibitors in plants are pretty much what a chemo therapeuticum means for cancer, i.e., rapidly dividing tissues will be affected most. Germinating seeds depend on mitosis for growth. An established plant will also be affected (it will stop growing), but it will stand its ground. To push the analogy - chemotherapy is often commenced after surgical removal or irradiation therapy to remove the tumor, and then chemo is applied to make sure any surviving tumor cell will not start to divide. Your herbicide will prevent germination (cf. cancer re-growth), but will not grossly affect established plants (cf. existing tumor).


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Are abrasions considered closed wounds?
A closed wound is one where skin is intact and underlying tissue is not exposed to the environment.
Abrasion is an erosion of skin usually due to sheering force. In most cases the dermis is intact and the injury is superficial limited to epidermis. Abrasions heal without scarring by epithelialization.
Are abrasions considered closed wounds? I would think they are open wounds as the underlying tissue (which would be dermis in this case) are exposed to the environment. Please state the reason why they are classified into whatever group.

I beg to differ... I have a lot scrapes that have scarred.

The definition of closed and open wounds is variable. In histopathological terms (i.e. looking under a microscope) it is usually defined that a wound where the dermis is affected is open. In this case an abrasion is an open wound. This puts it in the same class as cuts (incisional/lacerations), tears and punctures. Closed wounds on the other hand are when the dermis isn't affected, such as in a haematoma (blood collection under the skin) or crush injury (extreme force typically for a long period of time) and contusions (i.e. bruises).
Medically they may be divided by management. Where open wounds are wounds which are likely to be contaminated and need thorough cleaning and may need antibiotic cover whereas closed wounds are ones that are very unlikely to be. In this case, abrasions may be considered a relatively closed wound as not all the protective layers of the skin have been breached (the dermis is not completely breached). Thus the physical barriers are relatively intact and continue to offer us defense against bacteria and organisms.

Thanks for the answer, so as long as the skin is not breached the wound is considered closed

Updated the answer to include pathological definitions :)