How can a virus be determined to cause a disease? How can a virus be determined to cause a disease?  From other posts I have read here, humans carry hundreds of different strains of viruses.  How is a study structured and carried out to determine that one virus is the cause of a disease, and not any of the other viruses present?  Any examples of studies are greatly appreciated as well.

A modified form of Koch's postulates is used to guide experiments that establish that a particular virus causes disease.

As a specific example of such a study, the SARS-CoV virus was determined to cause the SARS disease by fulfilling these criteria:

SARS virus is found in people suffering from SARS, and not found in those who are healthy.
The virus can be isolated from infected people and grown in cell cultures (here, Vero cells).
Viruses grown in culture can be reisolated and compared with (and found identical to) the suspected pathogenic virus.
This isolated virus can re-infect people (or infect model organisms; in this case, a species of macaques).
Virus in reinfected organisms can be isolated, grown in culture, and found identical to the original pathogen.
The immune system is observed to respond in similar ways to the infection (pneumonia and lung tissue lesions).


Can we really 'discover' 85% of mammalian viruses? This virology [blog] discusses estimates of the number of mammalian viruses and the costs of 'discovering' 85% of them.

My question is whether this is not a forlorn hope. The ".632 rule" in statistics says roughly that as we approach n random samples from a large population of size n we will see only about 62.3 per cent of the population. After a point we would begin to see the same viruses again and again. This argument is probably stronger with respect to marine viruses, as they may be even more numerous and sampling at depths could be difficult.

I wonder if someone with experience sampling small organisms from large populations or familiarity with the literature has an idea about the plausibility of seeing 85% of a large population, such as mammalian viruses, by sampling?

If the samples are really random (in some sense) and the population is large, a few computer simulations reveal the power of this rule of thumb.

Edit in response to comment/question:

Like any such estimate, the blog's estimate of 3.6 million is a guess. I am not reproducing the calculation here because it's just speculation.

Having said that, if 3.6 million were correct, we would have to draw about 6.8 million samples to find 85% of the existing viruses, 8.2 million to find 90%, and so on. As the blog notes, the PCR approach detects viruses similar to those we know, so the sampling is worse than random. If we look at the difficulty of finding/using a method that has a reasonable chance of capturing any of the extant viruses, the number 3.6 million looks very big.

For some statistical models, see e.g. The Mathematics of Biodiversity (Part 1) by John Baez.

However, in terms of new species, such statistical methods may not suffice - usually also our tools for discovering change. So it might be more accurate to extrapolate number of some kind species we know as a function of time.

For extrapolations (though not for viruses) see e.g.:

Camilo Mora et al., How Many Species Are There on Earth and in the Ocean?, PLOS Biology (2011).

In any case, for viruses (and many other fast-multiplying asexual creatures) defining number of species can be anywhere from tricky to impossible (for fundamental reasons, not only - practical). At best you can try to estimate their time to the last common ancestor. See also links in this discussion on Azimuth.


Do you know of any disease where HLA / MHC association discovery has led to better treatment or management? If we discover an association between a disease and a particular HLA type (MHC class I or class II molecule) then it may provide us with some insight into the disease in a very basic way. However, will it provide us with a therapeutic target? Or second best, will it provide us with information that is useful for diagnosis or management? I am looking for examples. Do you know of any?

The most obvious is in transplantation where one would use HLA typing to match donor to recipient but that is not the same as using knowledge of an HLA type to target, treat, diagnose, prognosticate.

I don't know any true disease associations, but since this question still has no answers, I'll offer one...

One class of associations you might be missing is difference in drug response. Patients with HLA-B*5701 are known to be hypersensitive to abacavir. Genetic screens are available to screen for this allele, and this information is used clinically.


Inverse of dopamine reuptake inhibitor? The wikipedia article on the dopamine transporter gives examples of some drugs whose effects are mediated by the inhibition of the dopamine transporter, such as cocaine and amphetamines.  Are there any drugs or substances whose mechanism of action involves increasing the activity of the dopamine transporter, i.e., a "DAT releaser?"

It's important to note the difference in mechanism between cocaine and meth. While cocaine blocks reuptake, meth makes VMAT - vesicular monoamine transport - leaky and actually reverses the transportation of dopamine, so that instead of transporting dopamine into the axon terminal, it actually transports dopamine out as it leaks from the vesicle that carry it. This is what is meant when referring to 'reverse transport' of dopamine through DAT. Feel free to read this abstract and the sources it cites (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631950/).

Regarding the possibility of a DAT agonist of sorts, looks like current research has identified some potential targets. One of which seems to be luteolin and its derivatives (http://www.ncbi.nlm.nih.gov/pubmed/20971650). Current studies find new derivatives and test the EC50 to assess pharmacological efficacy.


Can general soap kill bacteria? I have read that general soap can kill bacteria by opening holes in the bacterial membrane.

http://questions.sci-toys.com/node/90

However, I found some articles as well saying that it cannot.

http://goaskalice.columbia.edu/answered-questions/does-soap-kill-germs

There seems split answers among experts,
so I would like to know which one is correct.

Could anyone advise me?

Thanks.

Soap kills nearly all the bacteria it comes into contact with by dissolving the bacterial membrane.  Some viruses with protein coats can resist soap, but many viruses have similar membranous coats (like HIV) and are usually disrupted by soap.  I'm sure it washes some away too, but to say they don't kill bacteria is misleading. In the end, though, they are gone.

Antibacterial soap with triclosan does not kill bacteria on contact and are no more effective than if they had no triclosan at all.  That's actually a good thing since really using an antibiotic would probably accelerate antibiotic resistant bacteria which is a serious - probably catastrophic public health failure. A recent study showed that killing bacteria by soaking with triclosan took 9 hours to start showing an effect.

To achieve full sterility, surgeons bathe their gloves in iodine (see details in the comments below) and their instruments will be sterilized by heating them beyond the boiling point in an autoclave under pressure.   That's useful when you are breaching the skin in surgery, but the skin needs some bacteria to be healthy long term and works well to fend off bacterial infections.

Your confusion seems to come from finding a page full of errors. Alice didn't really do her homework.


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

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

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

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

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

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

You can use whitespace in rest of the two columns.

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

How to find nearest genes without using Peakanalyzer?

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

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


What is the scientific name of this lovely orange black flying beetle? Found on Rangoon creeper (Combretum indicum)

This is a blister beetle from the species Mylabris pustulata.

Here is another photo for comparison:

Source: http://www.knowyourinsects.org/Coleoptera1.html

And, just for fun, the specimen in my link and yours, side by side:

It's worth mentioning that Mylabris has been confused with the Genus Hycleus, and the synonymy is complex.


Effects of lactic acid ingestion What would happen if I drink lactic acid?

I use lactic acid to clean an espresso coffee machine and I wonder what injuries could occour drinking it.

No, don't drink it... And here's why.

Ingesting lactic acid or for some reason having too much of it in your body can cause a variety of health problems ranging from mild to deadly. There are two types of lactic acidosis; the first is called metabolic acidosis and the second is known as respiratory.

Metabolic acidosis - which is what would be caused by ingestion - occurs when the fluids in your body build up too much of the acid and your kidneys can no longer keep up with the demand placed on them. Or they over respond and remove too much base from your body, leaving you acidic.

Respiratory acidosis is caused when your lungs cannot effectively remove CO2 from the blood. A buildup of CO2 leads to a more acidic body chemistry.

Regardless of what the cause of the acidosis was, you can expect some of the following.

Symptoms of metabolic acidosis:

~Rapid and shallow breathing

~Confusion

~Fatigue

~Headache

~Sleeplessness

~Lack of appetite

~Severe acidosis can cause shock, organ failure and even death

Diagnosis of acidosis:

A series of blood tests will check calcium, sugar and electrolyte concentrations in your blood.

My sources for this information:

Healthline

WikiPedia on Lactic Acidosis


Germ cells vs. gametes Naively, I thought that germ cells are diploid (in diploid species like human/mouse at least). Then, germ cells undergo meiosis and become haploid. I thought this was the critical change that defined these derived cells being named gametes (spermatozoon/ovum) rather than germ cells. However, I read that while XX mammalian germ cells undergo meiosis during embryonic development, XY germ cells don't go through meiosis until well after birth (puberty). This would mean that female gametes arise over a decade before male ones in humans. Is there an accepted definition of when germ cells differentiate into gametes and the terminology?

Your observation is right.

In females( having  XX mammalian germ cells), Oogenesis starts with
the process of developing primary oocytes, which occurs via the
transformation of oogonia into primary oocytes, a process called
oocytogenesis. Oocytogenesis is complete either before or shortly after
birth.(1)

The "germ cells" are called oogonia. Ovum is not a direct product
of meiosis I, the oocyte forms a primary oocyte in meiosis I, which
undergoes meiosis II after fertilization to give an ovum.

The ootid is the immature ovum formed shortly after fertilization, but
before complete maturation into an ovum. Thus, the time spent as an ootid is
measured in minutes.              ....(2)

(In oogenesis, the ootid doesn't really have any significance in itself, since it is very similar to the ovum. It matures into an ovum.)
This diagram sums it up very well:

Oogenesis in Eukaryotic Cells.(A) oogonium where the mitotic division
occurs (B) differentiation and meiosis I begins (C) primary oocyte (D)
meiosis I is completed and meiosis II begins (E) secondary oocyte (F)
first polar body (G) ovulation must occur and the presence of the
sperm penetration (fertilization) induces meiosis II to completion (H)
ovum (I) second polar body               ...(3)

It is commonly believed that, when oocytogenesis is complete, no additional primary oocytes are created, in contrast to the male process of spermatogenesis, where gametocytes are continuously created.

In males, again, as you say, Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. The germ cells here are the spermatogonia. But here, initiation of spermatogenesis occurs at puberty. So, males start producing sperm when they reach puberty, which is usually from 10-16 years old.(4)

(The process is almost similar to oogenesis, I would recommend you to start with the wikipedia page if you want to understand this in detail.)
Take away points:

The first haploid cell formed from a diploid germ cell is not an ovum/spermatogonia.

Ovum is formed after fertilization, whereas sperms are formed at puberty.

Oogenesis starts after birth, whereas spermatogenesis starts at puberty.

1- https://en.wikipedia.org/wiki/Oogenesis
2- https://en.wikipedia.org/wiki/Immature_ovum#Ootid
3-https://upload.wikimedia.org/wikipedia/commons/1/1a/Oogenesis.svg
4- https://en.wikipedia.org/wiki/Spermatogenesis


Are there human-ingestible liquids that do not contain water? My son asked me a question that stumped me: Is there anything a human can drink that does not contain water?

It stemmed from a conversation in beverages in general where I was pointing out that they all are based on water...coffee, soda, milk, etc.

That's when he asked if there are any beverages that don't contain water. Given that nearly all of the water and even solid food I could think of contains water, I couldn't come up with anything, but now I'm curious about it to so came here to ask the experts!

Is there anything a human can drink that does not contain water?

Yes, there are a lot of liquids that do not contain water, but mostly they are not safe for human consumption.

Mercury is a liquid at room temperature. Can a person swallow it? Most assuredly. Motor oil has no water in it. It's not a satisfying beverage. Canola oil, olive oil, and many other food derived oils can be imbibed in even reasonably large amounts, but it won't do your digestive tract a big favor.

I've treated goats with propylene glycol (a liquid), parents treat their kids with mineral oil for constipation, etc. etc.

It depends on what you mean by "drink".


Can one use dialysis tubing several times? I would like to know, if one can use dialysis tubes multiple times. Or is there a risk of plugging the pores? I use the tubes for dialysis of a solution that contains a precipitated enzyme (183 kDa) and ammonium sulfate (132 Da). Thanks!

This is more of a long comment than an answer, since I don't know. It could be okay, but if you are unsure whether it will work, is it really worth the risk? Here are some thoughts:

With high AS concentration, there is an initial large influx of water which can stretch the tubing. If this is repeated several times you may stretch the pores to where they no longer retain your protein. You can determine yield after each dialysis to see if loss increases with use.
Clogging up the pores seems like it could plausibly happen. You could add some low molecular weight dye to monitor whether the membrane remains permeable with use.
Dialysis tubing costs like 5 ¢/cm. Unless you're using 10 meters at a time, it's really very cheap.


Could the proteome of E. coli be fluorescently labelled? What proportion of the total number of proteins in E. coli could be fluorescently labelled for PALM/STORM imaging?

One at a time, you could potentially label all of them.

If you're asking how many proteins you could label at once, your biggest limitation is probably your microscope. In order to distinguish between different types of proteins you need different color fluorescent labels (dyes, fluorescent proteins, etc). Even the fanciest fluorescent microscopes tend to be set up to excite/record labels in <10 distinct wavelengths.

In practice I've only seen experiments where there were tracking 3 distinct types of proteins at one time.


Why do we urinate more when we are nervous? This question is a result of my personal experience... But I guess that is common for many of us.

My school timing is 8:00 am to 1:30 pm (usually). During normal school days I typically urinate one time - at most. Last month when we were having our practical exams. There was a fair amount pressure to score high marks and on top of that we did not have any experience with such exams.

On the day of the exam; I was a little nervous about it. The duration of the exam was 3 hours (from 9:00 am to noon) on this day I urinated 4 times.

Several of my friends also experienced the same thing.

I was nervous also because for two days before the exam I was afraid that I hadn't even touched any book. I was thinking that there was no way I could cover the whole book and so I didn't even touch them.

Now that I have final exams in about two weeks, I was revising my syllabus but for the last 4 days I'm not touching the books. Whenever I start solving problems from any chapter then I have to look back for the formulas. Questions in which reasoning is asked, I love to do that. I'm not very good at memorizing things and so when I compare myself to my classmates then I feel like I don't know anything and so I give up. I have never tried to memorize anything, but I understand the reasoning and the concepts.

Kindly give me the answer of the question.

I found an interesting article that dealt with anxiety and micturition. There are no proven or accepted view on this. There are a few theories as to how this happens.

I am quoting it:

  There are several beliefs for what causes frequent urination from anxiety, and the likelihood is that all of these factors play a role:

  Muscle Tension – This is one of the most likely causes of frequent urination. When you have anxiety, your muscles get very tense. This tension puts pressure on your bladder, which in turn makes you feel like you need to urinate more than you would otherwise.

  Evolutionary Adaptation – Another theory is that there is an evolutionary reason that frequent urination would be advantageous. Remember, anxiety is the misfiring of your healthy fight/flight system. In times of fear, urination may keep the body lighter by losing extra weight, making it easier to flee.

  Light Overload – It's also possible that, because anxiety is a misfiring of the fight/flight system, your body may simply be lightly overloaded. The fear is not intense enough to cause immediate urination, but it may make it harder for you to feel like you can hold it back.
  Also, those with anxiety are more prone to focusing on different sensations unintentionally. There are often times when you may feel the need to urinate slightly but your body has no problem ignoring the feeling and holding it back. With anxiety, it's possible that your brain is focused on the sensation, potentially causing you to feel like you need to urinate more than you do.

  Finally, anxiety can also change your body chemistry, altering your digestion and changing the way you process nutrients. That may cause more water to pass through your body.

Source:http://www.calmclinic.com/anxiety/signs/urination-problems


In what situations, when reacting to impressions, are the signals sent directly from the thalamus to the hypothalamus? Normally when humans react to impressions, signals are being sent through different centers in the brain through the chain of:
Impression ${\rightarrow}$ Thalamus ${\rightarrow}$ Cerebral Cortex ${\rightarrow}$ Hippocampus ${\rightarrow}$ Amygdala ${\rightarrow}$ Hypothalamus ${\rightarrow}$ Reaction

In some situations, the middle parts are skipped, handling feelings, long-term memory and understanding. The chain in the case consists of:
Impression ${\rightarrow}$ Thalamus ${\rightarrow}$ Hypothalamus ${\rightarrow}$ Reaction

Under what circumstances does this alternate path of reacting happen, and what effect does it have on the outcome of the reaction?

As @Pyssling states, it has to do with fear, and how we process situations that are potentially dangerous. There is a distinction between the two concurrent processes that you describe, that go under the title "short route vs long route" or "low road vs high road" (possibly more titles).

The short route (or low road) is the immediate process/reaction/response, which would enable os to avoid death in certain situations - This works on an instinctive level. The long route (or high road) is the process/reaction/response that could be defined as a thorough evaluation of the input/signal that we receive.

This site has descriptions and images that can be read on three "levels of explanation", and I find them highly informative.
http://thebrain.mcgill.ca/flash/a/a_04/a_04_cr/a_04_cr_peu/a_04_cr_peu.html

Here is a youtube video on the subject "How fear is wired in the brain" that deals with the same topic. https://www.youtube.com/watch?v=vl_B6nz3UOQ

I am in no way an expert and have stumbled upon these sites based on personal interests, so I do not know if someone may be able to criticize their validity / quality, but I found them excellent.


How exactly do mosquitoes navigate directly on target? There is a question on mosquito orientation in darkness, however the answer does not address it very specifically and I'm more interested in mosquito ability to lock on target than general navigation.

I know that they use their antennae to detect CO2 and lactic acid. However smell alone doesn't seem good enough for precise landing.

They do have eyes, however they can operate in complete darkness which means the eyes are redundant system for the attack.

They can sense heat, but they do not seem to attack non-fire based heat sources.

So how exactly does a mosquito succeed to land on piece of uncovered skin? Does this tell us anything about interfering with their navigation system?

Mosquitoes do not rely on a single cue to find its host. It is the combination of CO2, temperature and odor cues, that makes mosquito an efficient blood feeder.
 These two papers might help you in understanding how mosquitoes target their hosts.

Genetic analysis of mosquito detection of humans

Multimodal Integration of Carbon Dioxide and Other Sensory
Cues Drives Mosquito Attraction to Humans


How much heat for how long to Kill RHDV? Rabbit hemorrhagic disease is caused by the Virus RHDV.  There are two verisions V1 & V2.

It is extremely devastating to both pet and wild rabbits.  With fatality rates reports of 75%+.

It is currently devastating rabbit populations in the US. There are a number of vaccines but non-are approved for use in the US.

I have been reading up about it and found this claim in a few places.

  RHDV is also reported to survive exposure to pH 3.0, heat of 50°C (122°F) for an hour Source

.

  It survives heat of 122F for one hour. source & source

My question is: How much heat for how long will kill RHDV?

Often, in studies of viral infection, heat-inactivated viral stocks are used as a non-infectious control.  See Matthaei et al. 2014 1 for an explanation of how such a stock was prepared for RHDV:

Heat-inactivated RHDV stock was generated by incubating the virus preparation in 2 ml screw cap tubes for 180 s at 85°C in a water bath to ensure a drop in infectious virus of more than 99.9%

The methods section for that paper cites a study by Duizer et al. 2 on the inactivation of caliciviruses (which include RHDV).  Therein, the authors tested the heat inactivation of canine calicivirus no. 48 (CaCV) and feline calicivirus F9 (FeCV) at 4, 20, 27, 37, 56, 63, 71.3, and 100°C for time periods varying from weeks (4°C) to seconds (71.3 and 100°C):

Times required at different temperatures to achieve a 3 log10 reduction in viable virus titer (TCID50) in DMEM (3 to 4 μg of protein/ml).

Note that, in both studies, viral heat inactivation is carried out in liquid culture, where it is easy to obtain a uniform temperature by mixing.  For heat inactivation of RHDV on food/hay, rate and uniformity of heating will be different.
Citations

Matthaei M, Kerr PJ, Read AJ, et al. Comparative quantitative monitoring of rabbit haemorrhagic disease viruses in rabbit kittens. Virol J. 2014;11:109.
Duizer E, Bijkerk P, Rockx B, De Groot A, Twisk F, Koopmans M. Inactivation of caliciviruses. Appl Environ Microbiol. 2004;70(8):4538-4543.


Is mucus significantly affected by the presence of ions? In mucus, there is besides water and the mucins (Proteins for mucus), there are Ions like $Ca^{2+},Na^{+}$, etc. I have read that These Ions can Control the mucus swelling, i.e. the volume that the mucus occupies. Moreover, I have heard that some polymers can be affected by the presence of Ions, These are called "electroactive polymers". Is mucus a substance that changes ist consistence dramatically, when Ions are added or removed (equivalently, if pH value is changed due to $H^+$ ions)?

Yes.  Mucus is hydrated by the movement of ions.

Cells cannot move water.  Cells can only move ions, and water follows the osmotic gradient.  When hydrating mucus, cells move ions into the mucus and water follows.  A failure of this system is seen in cystic fibrosis.

Targeting ion channels in cystic fibrosis

  CFTR, the protein that is defective in cystic fibrosis (CF), directly
  mediates the transport of chloride and other anions through the apical
  membrane of several types of epithelial cells [1], [2]. Therefore,
  mutations impairing CFTR function cause a severe imbalance in ion and
  water transport that leads to a variety of negative effects in various
  organs. In the lungs, impaired secretion of chloride and bicarbonate
  appears to have multiple consequences. First, reduced secretion of
  electrolytes, and consequently of water, causes dehydration of airway
  surfaces with impairment of mucociliary clearance [3]...

People with cystic fibrosis have a defective chloride channel, and it cannot move chloride into mucus.  They therefore have thick mucus with abnormally low water content, and much of the trouble they have with their lungs is because this thick mucus does not perform its functions well.


Why do males have more birth defects? I taught in elementary school for 20 years and noticed that males were far more likely to be classified as handicapped than females.
More males than females die at birth and are more likely to have birth defects. Why?

Welcome to Biology.SE Wendy.

Issue in your post

There are a few issues in your post.

You made a personal observation that males tend to more often be diagnosed with a handicap than females (in frequency). You probably did not keep track of the numbers and you probably did not make any statistical analysis. So there is really no reason to trust this observation. The idea that males are more often classified as handicapped than females is opinion-based for the moment and you will need a reference for this before asking why it is true.
You also claim that most birth defects occur in males and not in females. You should also include a reference.
You are talking about gender difference in "handicap frequency" and "birth defect frequency". It is a little unclear what the question (your last sentence Why) refers to. Maybe both. In such case, why would you expect that a common mechanism explains both observations? You should probably restrict your question to one or the other only.

For these above reasons, the question cannot be correctly answered in its above form. But below is something that may already help you.

Birth defects

It is true that birth defects is more prevalent among males than among females (in humans). According to Lary and Paulozzi 2001:

  The overall prevalence of major defects at birth was 3.9% among males and 2.8% among females.

Reading their abstract only, one can see that they go on saying

  Defects of the sex organs were eight and one-half times more prevalent among males and accounted for about half of the increased risk of birth defects among males relative to females. Urinary tract defects were 62% more prevalent among males, and gastrointestinal tract defects were 55% more prevalent among males.

In consequence, it seems at first sight that the difference in birth defects frequency is very much related to the development of sex organs. In their abstract they announce that they discuss the mechanisms that account for such difference.

I currently don't have access to the paper (I am not on campus) to report more details of their findings.


How "exactly" is Rabies transmitted? Context: I know a person which has developed a sort of "phobia" with respect to touching things that has (even the slighest) chance of being in contact with something that can transmit rabies. For instance, if something (a coin) falls on the floor of our university, said person almost cannot take it, since dogs sometimes pass around the place. This has reached a severe level which hinders this person experience in life. However, there is apparently some hope of rationalization. Specifically, the person told me that if someone can prove, for example, that the virus do not "live" long enough after dropping from the saliva of a dog to the floor in order to be transmitted to a human being, then maybe she will be more relieved. This led me to search for information on the internet, but nothing was conclusive. This takes me to my question, and sorry for the sidetracking.

Can someone be infected by rabies by merely taking something from the ground where a infected dog may have passed by? How long does the virus "live" (or is active, I don't know the  proper term) after being "exposed" to the environment? More generally, how exactly does the process of infection happen, and how can it happen?

This is actually far more complex a question than you probably know. The country you are writing from matters. There are some rabies virus variants that have a relatively low pathogenicity for humans (dog rabies is one of these; a relatively large innoculum is required, i.e. a bite, commonly a deep one with lots of virus-laden saliva.) The likelihood of canine-associated rabies developing from a non-bite exposure is extremely low; in fact, the exact risk is unknown.
In the US, enzootic (dog-to-dog) canine rabies virus has been virtually eliminated through vaccination and stray control programs, making wild animals (including feral cats) the primary concern. Depending on the country your friend lives in, dogs may not even be high on the list of worrisome sources.
Regarding canine-associated rabies,

Rabies control was accomplished [through dog vaccination programs, responsible pet ownership, and serious population control of stray dogs] in Europe, North America, Australia, Japan, Taiwan, Malaysia, and Singapore.

If you don't live in one of these countries/continents, dog-associated rabies is still a major concern. If you do live in the mentioned areas, you can probably dip your hand in dog saliva and not be concerned.
Rabies is usually contracted by a bite; that is most common.

The most dangerous and common route of rabies exposure is from the bite of a rabid mammal. An exposure to rabies also might occur when the virus, from saliva or other potentially infectious material (e.g., neural tissue), is introduced into fresh, open cuts in skin or onto mucous membranes (nonbite exposure). ...Exposures to bats deserve special assessment because bats can pose a greater risk for infecting humans under certain circumstances that might be considered inconsequential from a human perspective.
how exactly does the process of infection happen, and how can it happen?

The exact way it happens is not completely understood, but that answer won't help you convince your friend of anything. The virus is usually deposited in tissue near a cutaneous (peripheral) nerve. If it gains entry to the nerve, it makes its way to the brain with the typical disastrous results.
Having said all this, your friend is not going to stop worrying, because the virus is only the focus of an irrational fear. Though the foci of irrational fears are fairly stable, OCD is most likely the underlying problem, and conventional rational discourse doesn't really suffice in curing the obsession.
During 1990-2007, 34 bat-associated human cases of rabies were reported in the US: 6 cases reported a bat bite; 2 cases reported a probable bite; in 15 cases, physical contact was reported (e.g., the removal of a bat from the home or workplace or the presence of a bat in the room where the person had been sleeping), but no bite was documented; and in 11 cases, no bat encounter was reported, but the rabies virus was bat-specific.
Any encounter with a bat, even a dead one (as stated above), must be evaluated for possible post-exposure prophylaxis.
Unfortunately, in the US, animal rabies is common, and at least 23,000 persons/ year receive rabies postexposure prophylaxis (PEP). (It is probably considerably higher, as no reporting mandate exists.) With the elimination of canine rabies virus variants and enzootic transmission among dogs, human rabies is now rare in the United States, with an average of one or two cases occurring annually since 1960.
In the US in 2013, of the three human cases reported, 2 were involved in organ transplants (raccoon rabies virus variant) and one was a Guatemalan (canine rabies virus variant).
In 2012, one human died from an exposure to a bat. He touched a bat under a bridge. He did not report a bite to a witness. He became ill while traveling, and died in Switzerland. A number of humans exposed to his saliva (including his Swiss caregivers) received PEP.
*Some people in high-rabies areas without the illness have been documented to have developed antibodies to rabies. The mechanism is unknown.
Human Rabies Prevention - United States, 2008
Pathogenesis of Rabies
A Single Amino Acid Change in Rabies Virus Glycoprotein Increases Virus Spread and Enhances Virus Pathogenicity
Human Rabies Prevention (Comment From a Canine‐Rabies‐Endemic Region)
Epidemiology of rabies post-exposure prophylaxis—United States of America, 2006–2008
Rabies surveillance in the United States during 2013
Use of a Reduced (4-Dose) Vaccine Schedule for Postexposure Prophylaxis to Prevent Human Rabies: Recommendations of the Advisory Committee on Immunization Practices


Is this European(western), Eastern(northern) or another Hedgehog? Yesterday this little guy ambushed my bicycle, thankfully tire-hedgehog contact was avoided at the last moment. Now I am wondering which one is it. Going by wikipedia maps and photos it should be either European/Western (Erinaceus europaeus) or Northern (E. roumanicus).

Sadly due to nocturnal nature of Hedgehog, "smart"phone camera and general willingness of Mr. Spikey to quickly leave area of incident this is best photo I have:

Incident occurred in Poland, Europe, around 21:30 local time.

I think the picture you have is not enough to make a proper distinction between the two species.

By this site, they found some morphological characteristics to make the distinction but:

You have to carefully take pictures of the animal parts
The study nearer Poland has been made in Estonia and those characteristics could be slightly different in other countries.

I did not find another documents about hedgehog populations in Poland but the wikipedia page says both species are living in the country.


Altering the human genome I recently had a conversation with a rather unusual gentleman who was, let's say, more than a little partial to conspiracy theories. He has this idea that governments are lowering "nanowires" from drones, to inject people with chemicals that modify their genetics in order to reduce their lifespan dramatically, or change their opinions and thoughts.

Clearly this man was a fruitcake, and the complexities of his psychology probably warrant a whole separate debate, but he did get me thinking about the theoretical side of how such a thing might be done.

So, as such, I have a few questions on the matter:

Is it even theoretically possible to alter human genetics using only an injected substance? I'd imagine trying to get a single DNA change to propogate through the entire body without being killed off by the immune system would be near impossible.
Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems, cancers, high blood pressure, strokes, etc), is it possible to modify human DNA to create these issues in a living person?
Has much research gone into how genetics affects thought and opinion, or the way we perceive and react to situations at an emotional level? If so, is it theoretically possible to alter this at a biological level?

I'm certainly not advocating any of this, and I apologise for the unusual nature of the question, but it's something I certainly find interesting to think about!

Concerning the first question, it is very well possible to alter human genetics by injecting a highly radio-active substance that will eventually cause mutations almost all cells. The lifespan will be dramatically reduced, however and the condition is known as "radiation sickness"(link to Wikipedia).

But the person probably means so-called "directed mutations" (link to Wikipedia), when the changes of genetic information is not random, but rather at a certain place and towards a certain function.

Second point, this is the area of extensive research: if we could specifically cure a gene than many diseases that are incurable now (like cystic fibrosis) could be effectively treated.  The complete nanotechnology (link to Wikipedia) is all about it.

As to the third point, this is also a very old discussion about the role of nature (=genetics) and nurture (environment). Answering this question in the scope of other questions I can suggest that (genetic) knocking-out some inhibiting receptor systems in brain can lead to certain malfunctions and deceases, including the lymbic system that is responsible for emotions and perception.


Does freezing microorganisms such as probiotics kill them? Does freezing microorganisms such as probiotics kill them?  If not, what is the process that allows them to "come back to life" after the temperatures are increased?

As an example, lets say you freeze a yogurt (whether it be Greek, Australian, Turkish, Indian, Russian, European, or Western) and eat it while frozen.  Would the probiotics in the yogurt "come back to life" and be beneficial?

Specifically, I am referring to freezing refrigerated yogurts, and not products that are sold as "frozen yogurts".

What's the biological basis for this?

Yes, they do. For a look at survival of Lactobacillus and other bacterial species after multiple freeze/thaw cycles, check out Harrison 1955 (below).

The awesome hand-drawn graphs show that many bacteria survive after being frozen for 11 weeks. There's also a figure on the following page showing that many bacteria also survive after multiple freeze-thaw cycles, but I won't include that page here for brevity.

Prof. Don Schaffner of Rutgers also supports this conclusion:

  So it's possible, even likely, that frozen and thawed yogurt will contain
  living lactic acid bacteria, although it may only be 10% or 1% of the
  total number of bacteria that were there before the yogurt was frozen.

I couldn't find a great deal of official resources on the topic, hence the paper from 1955 and random quote from a food science professor. However, in a lab setting, scientists regularly freeze bacteria and even eukaryotic human cell lines. Usually scientists use a cryoprotectant like glycerol, but many foods (like yogurt and ice cream) may contain an FDA-approved cryoprotectant (Wikipedia):

  One recent, successful business endeavor has been the introduction of [anti-freeze proteins] AFPs into ice cream and yogurt products. This ingredient, labelled ice-structuring protein, has been approved by the Food and Drug Administration.

So, yes, at least some of the bacteria in your frozen yogurt are still alive, and will have whatever beneficial/harmful/lack of effect when you ingest them.

Judging from figures 1-3 above, bacterial survival depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range. Also, it doesn't matter whether you thaw it first or eat it frozen as far as bacterial content is concerned, the bacteria will be unfrozen either way when they reach your digestive tract.


Can animals like squirrels leave "gifts" or tribute for humans? I've heard anecdotal reports of squirrels bringing up gifts to a person's house after that person left out food for them. Sounds bizzare and unbelievable, until I actually saw some kind of a nut right on the welcome mat in front of the door. I moved it and saw that it was eaten (shell fragments) a couple days later, telling me that it was actually a good nut.

This makes me ask - is this just a coincidence, or do some animals, like squirrels indeed offer gifts or tribute to humans?

I'm aware that cats frequently bring killed animals to human doorstep:

  By leaving a dead animal on the back porch, your cat is acting out its
  natural role as mother and teacher. You, her loving owner, represent
  her surrogate family. And frankly, she knows you would never have been
  able to catch that delicious mouse on your own.

However, for squirrels there's no domesticated relationship, humans are not a part of their family. Why would this behavior take place?

I believe a lot of these behaviours can fall under the umbrella term of reciprocity, or  reciprocal altruism.

  In evolutionary biology, reciprocal altruism is a behaviour whereby an
  organism acts in a manner that temporarily reduces its fitness while
  increasing another organism's fitness, with the expectation that the
  other organism will act in a similar manner at a later time (...) The concept is close to the strategy of "tit for tat" used in game theory.

For example, red-winged blackbird males help defend neighbor's nests. There has been some discussion around the reasons for this behaviour, but it has been observed that males reduced the amount of defense given to neighbors when neighbor males also reduced defense for their nests. Since kin selection doesn't seem to be an important factor here, this would support a tit-for-tat strategy (animals help those who previously helped them).

Some primates do this frequently too:

  A monkey will present its back to another monkey, who will pick out
  parasites; after a time the roles will be reversed. Such reciprocity
  will pay off, in evolutionary terms, as long as the costs of helping
  are less than the benefits of being helped and as long as animals will
  not gain in the long run by "cheating" – that is to say, by receiving
  favours without returning them.

The example with the crows, mentioned in the comment, can be interpreted under this light too. Those crows seem to give presents expecting something in return (albeit delayed!).

What's interesting though is that altruism, at first sight, would seem to go against reproductive success. Group Selection, however, is something Darwin was already talking about in Origin of the Species.

So, back to squirrels. I didn't find particular research about them in their relationship with humans (will keep looking), but analysing it under reciprocal altruism it could be justified that they give nuts expecting a potential future benefit for them or their group. There's much more to this complex dynamic, but reciprocity is definitely a strong candidate for explaining your kind gift-presenting squirrels.

Some quick references and materials:

The evolution of reciprocal sharing
The Gift, by Marcel Mauss (complete online book) --> From an anthropology point of view, Mauss was the first one to talk about recicprocity as economics. Absolutely recommended read.
Social semantics: altruism, cooperation, mutualism, strong
reciprocity and group selection


Is DNA mutation locally energetically stabilizing the DNA molecule I am no biologist, but as a physicist, a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system, at least locally. So I wonder if any research has been done along these lines for the DNA.

a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system

Why do you think that? Because it’s an endothermic reaction?

Consider that mutations don’t happen “just like that” (at least to my knowledge) –they are triggered by external energy influx from things like reactive oxygen species or ionising radiation. So yes, they cost energy but that energy doesn’t come energetically unstable chemical bonds; it is supplemented from external sources.

So it’s not necessarily true that mutations produce lower-energy chemical bonds.


A colony of humans are sent to an alien world, at what point would the descendants evolve to be genetically incompatible with Earth humans? I recently heard about the evolution of the London Underground mosquitoes, and how they have changed genetically enough that they almost can no longer reproduce with above ground mosquitos. Since this change in the mosquitos occurred over a relatively short time frame, how many years/generations would it take for a similar process to happen with humans?

The thought experiment that comes to mind is this. Assuming we sent a colony of humans to a distant planet and didn't have any physical contact with them for x number of years, how many years would it take for the colony of humans to branch off enough genetically to be no longer be able to reproduce with Earth humans? This is assuming the planet is habitable but different enough to change the course of human evolution.

In other words, what would be an expected minimum number of years it would take for this colony's descendants to be removed from Earth humans to one day again be reunited and not be able to produce offspring between the now different species?

In other words, what would be an expected minimum number of years the would need to pass before they are reunited and are no longer enough of the same species to produce offspring together?

That's an interesting model, because mosquitoes are vectors for serious illnesses, so are pretty well studied.  One team of scientists are working on genetically altering mosquitoes in Africa to make them unable to transmit the parasite that causes malaria. As the mosquitoes breed, it spreads through the population. In an interview, the lead researcher stated:

  In the lab, we saw the mutation spread to more than half the population of mosquitoes we had living in cages. This happened in a time span of 12 to 16 generations of mosquitoes (each generation being between 18 to 30 days in the wild). So it's quite efficient.

12 to 16 generations for one mutation to spread to half of a contained population. In human generations, 16 = 320 years, and that doesn't take into account fertility rates, miscarriages, etc. (Not a problem for mosquitoes, I presume).

How many mutations would it take to make two humans incapable of reproducing without endangering their own health or fertility? Excluding all of the harmful mutations that might just result in disease or decreased fertility? And add to that that the males need to change as well as the females? No one knows.

Imagine a cystic-fibrosis type mutation (one gene) that increased the viscosity of cervical mucus such that normal sperm could not fertilize the egg. There would need to be another mutation in males that would make sperm stronger, or secrete an enzyme that breaks down mucus, or something to that effect. However, look at Cystic Fibrosis. People used to die before adulthood. Most men with CF are sterile. Women with CF, living longer now because of better care and treatment, are getting pregnant, but many have a decreased lifespan post-pregnancy, and almost all the babies are premature. You can't predict "when" a series of beneficial mutations so dramatic as to change a being so dramatically. The answer might be never.

Try to give me a single or a few mutations that would prevent the ability of people from one population and another to mate. Say one mutation led to a smaller pelvis. Most women with that mutation would die in childbirth before a mutation arose to make smaller babies (which would most likely be a deleterious mutation as well).

I am not a geneticist (which is really the person who should be answering this question) but I think the odds of this scenario ever occurring are very low. I just can't imagine mutations making reproduction impossible between two populations being beneficial and selected in one population rather than harmful. Keep in mind that different humans from populations that were isolated for many thousands of years have no problem reproducing.


Which part of oranges contain fiber? I think it's pith, but here (non-english country) many chef suggest orange's vascular veins which look "fibrous" and have similar translated word with "fiber" itself.
Please enlighten me which?

Cellulose is one of the most common sources of fiber in the nutritional sense. Because oranges are plants, their cells have cell walls, made out of cellulose, so some of the fiber in an orange is surrounding each individual cell. Both vascular cells and pith cells tend to have particularly thick cell walls, so they are probably higher in fiber (this article also suggests that the pith is particularly high in fiber - vascular tissue is probably not mentioned because it is less prominent).


Male-Male competition limited to breeding season? I'm currently reading about sexual selection in the context of evolution. Unfortunately, the focus is always on animal behavior during the breeding season. What is 'normal' behavior outside of breeding season?

For instance: Red deer compete with their antlers. Are they doing that throughout the whole year, or just specifically during breeding season?

More general: Does male-male competition exist outside of breeding season?

It's strongest in the breeding season but male-male competition exists outside of the breeding season too, e.g. European Robins only breed in the summer, yet maintain territories year-round. It's pretty circumstantial, however sexual competition will only exist in the breeding season.

To address the Red Deer example, the deer only compete with antlers in the breeding season, but outside of the breeding season they aggregate in same-sex groups too, so most of the competition males will experience is male-male.

Normal behaviour will depend again on the species. Most birds I can think of have discrete breeding seasons and behaviour outside of this is rarely dependent on sex, generally including foraging etc. However I can think of many examples to this, such as Capercaillie, where the hens sometimes forage together. I suppose that 'normal' behaviour could be defined as any behaviour that is not part of the organism's motivation to reproduce.


How can I get the coding region from gene sequences? So, I have a file with 600+ sequences of a gene, each one from a different population. This file was obtained after blasting the chromosome sequences against the gene sequence. However, I need the coding regions as well. Should I do the same and blast the chromosomes against the exons, or should I blast the gene sequences against the exons?

Not all the exonic sequence is coding. The ends have 3' and 5' UTRs.

Can you find gtfs for your organism?  Those would be easier to work with.

Or, I'd do blastx against the protein, that should pull out just the sequence that codes for protein.


Making new antibodies Is there a model of how the B-cell-antibody pool in the lymphoid organ evolves during the first two weeks of infection by a new virus ? With a model I mean something like this

  At first we have $10^6$ different antibodies binding weakly to 4-5 amino acid  motives and through somatic hypermutation and selection the pool converges to a few dozen of antibodies binding strongly and specifically to some 8-10 amino acid  motives in the most numerous antigens presented by T cells (mostly motives found in the viral protein sequence since they must be in the peptide presented by antigen presenting cells).

This is what would make sense from the algorithmic point of view, which is often valid in biology, but not always. I have a few refs 1 2 3 but they stay elusive on that point.

If there is no such model then please make a few expert guesses.

There are plenty of papers with models for this. For instance, check a few hundred here.

Edit: I'm not an expert in modeling these particular processes. However, I do know about mathematical models in biology more generally. The OP asked if there is "a model" of how the B-cell antibody pool matures ('evolves'). The short answer is 'no'. There is not 'a model', because anyone can make their own model, with their own assumptions, parameters, methods, etc. The 'algorithmic point of view' is not something that is valid on itself, it is only useful (sometimes). It is the job of the modeler to navigate the nuances of her/his own model so that it ends up being useful for some particular purpose or question at hand. Thus, there is no simple answer to this question, or any other modeling question (take, for instance, all the talk about epidemic models in the COVID-19 case: even experts differ about the relevance of some particular details/assumptions). This is my long answer.


How does sugar enter neurons if they don't use insulin? I heard somewhere that as opposed to other cells, neurons do not use insulin to get their sugar supply.

Why is that?

What is the alternative mechanism? I assume sugar can't just enter the cell without some kind of help from a protein, is that true?

Insulin is not directly involved in sugar uptake. It accelerates sugar uptake by upregulating glucose transporters and activating glycogenesis.

Neurons have many glucose transporters including GLUT1 and GLUT3 which are responsible for glucose uptake.

Moreover, insulin being an endocrine molecule has effects throughout the body including neurons. So neurons need not secrete insulin.


Is protein production doubled if you have homozygous dominant genes as opposed to heterozygous genes? At school we were taught in quite simplistic terms. We were told that there is a dominant and recessive type of every gene and that if the dominant gene was present, the protein is produced and if it isn't, then a protein is not produced. We were just told that dominance was just an intrinsic property of some genes.

However, upon researching a little, I see that some genes are dominant because their corresponding allele simply doesn't make the protein but the dominant one does (please correct me if I'm wrong).

Does this mean that if someone is homozygous dominant for a particular gene, they produce double the amount of that certain protein as someone who has heterozgous genes or is there a mechanism that suppresses the expression of one of the dominant genes?

Dominance is defined based on the phenotype

Dominance is defined based on a phenotype of interest. Pick a phenotype, say coat color for example. If genotypes AA and Aa have the same coat color while aa has another coat color, then A is domiant over a.

The concept hold even for sequence that do not produce proteins

The concept of dominance can be applied to any locus which variance explains phenotypic variance, whether this locus codes for a protein or not.

Most sequences that affect the phenotype are regulatory sequences that do no produce any protein. In such case, your intuition that dominance is the allele that produce more proteins really does not make much sense.

Mechanism

A whole lot of mechanism can yield to such dominance relationship. It is not uncommon that the recessive allele comes from a loss-of-function mutation. In such case, yes it is likely that the AA genotype produce twice as many proteins as the Aa genotypes. But this is definitely not the only possible mechanism. Note that whether the number of proteins produced of the AA genotype is twice the number of protein produced of the Aa genotype, won't change anything to the phenotype of interest by definition of what dominant mean.

Dominance is actually pretty unusual

Most phenotypic traits actually result from the influence of several loci and allelic relationship at these loci are rarely perfectly dominant. Perfect dominance exist in reality but is definitely over represented in intro classes as they are simple to understand study cases.

Fitness

Note that there is a positive correlation between how recessive an allele is and how deleterious it is. It does not mean that the recessive allele is necessarily deleterious but there is a tendency.


What type of CCD system is required to take photos of luciferase I'm working with luciferase and I want to be able to take a photo of it. The trouble is, I can see the luciferase glowing in all of its glory in front of me but no matter how hard I try, I can't take a photo of the luciferase with my DSLR (Nikon D80).

I'm curious if I'm missing a certain lens or if I should be shooting using a different lighting setup. I'm already exposing for 30". Perhaps longer?

You are looking for a bioluminescence imaging device. These have very sensitive CCD camera and exposure times are around 5 minutes in complete darkness.


Meaning of a negative value for non-fiber, non-sugar carbohydrate based on a nutrition label One of the questions for my lab is to find the non-fiber, non-sugar carbohydrate per serving of an onion. Now the total carbohydrate for this onion is 11 g, the total sugars for the onion is 9 g, and the total fiber is 3 g.

11-9-3 = -1 g of non-fiber, non-sugar carbs for this onion and this is not making any sense to me.

The values on the nutrition label from the question (11 g total carbs, 9 g sugars, 3 g fiber) could be actually explained by rounding:

Total carbohydrates: 11.45 (rounded to 11)

Sugars: 8.55 g (rounded to 9 g)
Fiber: 2.55 g (rounded to 3 g)

...which would mean there are additional 0.35 grams of non-sugar, non-fiber carbohydrates...

...BUT...

...using such a label with only rounded values (and students not knowing the exact values), does not make it possible for students to calculate the amount of non-sugar, non-fiber carbohydrates.

So, another explanation is that there is an error in either total carbohydrates (11 g - too low) or in sugars (9 g - too high; more likely 6 g), according to NutritionData for 150 grams of raw onion:

Total carbohydrates: 14 g

Sugars: 6.4 g
Fiber: 2.6 g

In either case, it seems they have used a nutrition label that is inappropriate to ask a question about the amount of non-sugar, non-fiber carbohydrates in raw onion.


Are tongues red because they contain blood? Many animals have red tongues, though not all of them - blue-tongued skinks and giraffes come to mind. Are they red because of the blood (and therefore haemoglobin) in them?

It sounds plausible, but it also sounds like a post-hoc explanation.

I'd be especially curious about any other species having blue blood, like horseshoe crabs, but still having red tongues, unlike horseshoe crabs, which apparently don't even have tongues.

Mammalian tongues are red because of haemoglobin. Blue/black colouration is due to the additional presence of melanin.

  At the boundary between the epidermis and dermis are melanophores, cells that contain melanin. This brown pigment absorbs ultraviolet radiation from the sun that might otherwise damage the underlying dermal tissue. Melanin in the dark tongues of giraffes (Giraffa camelopardalis) protects the tissue from sunburn as the animals lift their heads into the top branches of trees to forage for leaves. In humans, synthesis of melanin increases upon exposure to sunlight and produces tanning. Extensions of melanophores reach into the epidermis where they inject their pigments into developing hair cells. In a few cases, such as the bright ischial callosities of baboons, pigmented patches of skin are used as visual signals. The blue and red coloration on the scrotum and perineal region of male vervets (Chlorocebus aethiops) is used in dominance displays.

From: Mammalogy: Adaptation, Diversity, Ecology by George A. Feldhamer, Lee C. Drickamer, Stephen H. Vessey and Joseph F. Merritt (2007) p 97 The Johns Hopkins University Press; 3rd edition edition


Which is the correct statement on proteins? I need help with one of the questions on my biochemistry assignment

Choose the correct statement on proteins:
a) proteins are folded by alpha-helix
b) proteins can preserve their function even if they only partially change their shapes
c) proteins are composed of amino acids
d) all of the above

Thanks in advance! :)

Do you have a textbook?  That will definitely have the answer early on in the chapter.  Also, have you tried reading the protein Wikipedia article, in particular the structure subsection.  You will find the information you want there.


How does chromosome cross-over occur? I have heard that during meiosis, homologous chromosomes from each parent "cross-over", which enables the off-spring to inherit some alleles from the mother and some alleles from the father.  The picture below illustrates this "cross-over", but of course this must occur at multiple sites, rather than just the one shown in the picture.

Now my question is what causes the chromosomes to align perfectly during cross-over so that the loci of a particular gene will substitute for the corresponding loci on the homologous chromosome, as opposed to being substituted with a completely random locus?  Does each gene have a unique non coding sequence before it specifying what gene it is to enable this process to occur?

Quite simply, because chromosome pairing is sequence specific. Holliday Junctions, which are the functional structures of a cross-over, occur through a process called "strand invasion," during which a region of one chromosome physically base-pairs with that of another.  Thus one locus cannot pair with a random locus, as there is generally insufficient sequence complimentarity between two random regions to form a functional Holliday Junction.  One interesting consequence of this mechanism is gene duplication and deletion in repetitious regions of the chromosome.  For example, genes with large repeated regions, such as the gene responsible for Huntington's disease, can expand and contract during homologous recombination due to strand invasion occurring at non-equivalent, but still homologous, sites.  Wikipedia does a nice job going over homologous recombination.  I also recommend looking over the relevant sections in Molecular Biology of the Cell, available on the PubMed Bookshelf.


What are the ploidy levels in major groups of organisms? If total number of chromosome in the cell is x, then for-example;

Are all animals diploid (x= 2n) ?

Are all fungi haploid (x= n) ?

Are all plants diploid (x= 2n) ?

Are all Protists diploid (x= 2n) ?

Also, what is the ploidy of archaea and bacteria?

Thank you very much.

Are all animals haploid (n=x) ?

No

  Are all fungi haploid (n=x) ?

No

  Are all plants diploid (2n=x) ?

No

  Are all Protists diploid (2n=x) ?

No

  Also, what is the ploidy of archaea and bacteria?

Generally speaking, Bacteria and Archaea don't have chromosomes (but have circular DNA). As such the question of ploidy does not really apply to them.

You might want to read about Biological life cycle to understand the terms haplontic, diplontic, haplodiplontic (and other similar terms).

Ploidy level can easily varies among species of the same family (typically in plants for which hybridization is common). There is no reason to expect that a taxon as big as "fungi" (for example) would all have the same level of ploidy.

Note that your question that all animals are haploids is surprising as you just described that humans are diploids.


Excretion of monovalent and divalent ions in sharks I have heard that sharks excrete $\ce{Na+}$ and $\ce{Cl-}$ by their gill surfaces but divalent ions like magnesium are excreted through feces. What could be the reason behind this?

The main reason seems to be a mechanism to save water and allow the excretion of higher concentrations of the ions. See the image (from here):

The urine enters the glomeruli at a relatively low rate and with a low magnesium concentration. The paper cited below mentions a concentration of 1.5mM. First organic compounds as glucose are recovered actively, water follows the molecules passively. Then more ions as Ca$^{2+}$ enter in the proximal segment II. In the distal segment finally sodium and chloride are actively transported out while water passively leaves the segment. The divalent ions (magnesium, calcium) are left in high concentrations (the paper below says that the Mg concentration is now around 130mM). This helps concentrating these ions for excretion while loosing as little water as possible at the same time. Sodium and chloride are actively regulated in the gills.

For a short overview, see the link at the image above, for a detailed view, have a look at the following publication: "Kidneys sans glomeruli".


Are there known life expectancy differences in non human mammals by sex? In humans either for biological or cultural reasons there are life expectancy differences by sex. But how about non human mammals? Are there known life expectancy differences in non human mammals by sex?

Are there known life expectancy differences in non human mammals by sex?

Yes, there are. It is not well studied in general, but for certain species it is. Here is a relevant excerpt (Austad, Fischer, 2016):

Females live longer than males in humans and all Old World monkeys and apes for which we have the best data. . . This appears to be true in both wild and captive populations. . .  Yet whether there is a general mammalian pattern of greater female longevity under protected, captive conditions where intrinsic physiological aging dominates mortality patterns, is not known because so few species have been rigorously investigated. What is known about the best described species indicates that all show a substantially different pattern from humans.

See the linked study for more information. There is a whole section on sex differences in lifespan in mammals.
In general, in any species where males fight fiercely amongst each other for status, I would also consider it likely that males have shorter lifespan on average than females. Although I don't have a good citation for this at the moment.
In a more recent review, Lemaître et al (2020) confirmed the tendency for females to outlive males across many mammalian species:

In human populations, women consistently outlive men, which suggests profound biological foundations for sex differences in survival. Quantifying whether such sex differences are also pervasive in wild mammals is a crucial challenge in both evolutionary biology and biogerontology. Here, we compile demographic data from 134 mammal populations, encompassing 101 species, to show that the female’s median lifespan is on average 18.6% longer than that of conspecific males, whereas in humans the female advantage is on average 7.8%. On the contrary, we do not find any consistent sex differences in aging rates. In addition, sex differences in median adult lifespan and aging rates are both highly variable across species. Our analyses suggest that the magnitude of sex differences in mammalian mortality patterns is likely shaped by local environmental conditions in interaction with the sex-specific costs of sexual selection.


Species Identification: Red velvety insect, India What species is this?

Description:

Location: India
These insects came out just after overnight rain.
They were all over the place.
Their body looks like velvet.

Are these insects poisonous?

As you might have noticed from its appearance, this is a red velvet mite. This is an arachnid (related to spiders) and not an insect.

The red velvet mite apparently does not bite or sting (according to this website), and it is also used for medicinal purposes in India, according to this Wikipedia image, so it is unlikely to be dangerous.

If you haven't seen it already, the webcomic The Oatmeal has an amusing take on some of the arthropod's mating habits.


Can you identify this climbing plant? In my house there's a strange plant that I see growing for years now. I believe it is a climbing plant. Do you know how is this plant named? Is it poisonous?

Location: Greece

Altitude: 800m.

Based on the fruits, leaves and tendrils, it looks quite like Bryonia dioica (which is toxic). It is almost certainly something from the same family (Cucurbitaceae, which often make such tendrils and usually have similar leaf shapes) and could even be the same genus, Bryonia, which is present in the Mediterranean region (there's even a cretica species). Based on images found on the internet, leaf shape seems variable (more or less indented).


Daphnis Nerii not moving Its been quite a while since my Daphnis Nerii has passed its eating phase, now its just a sort of recluse and is curled up in one corner and sleeps the whole day. It's a bit brownish in colour now. Although when I check on it, by lifting the container and moving it about, it starts jumping oddly. Like a jumpstart,  everytime it gets provoked. It maybe is the last phase of its instar period. Is it getting ready to pupate? Or is it not well?

Wikipedia tells us the following about the larva of the oleander hawk-moth (Daphnis Nerii):

  Just before it pupates, the oleander hawk-moth larva becomes browner in color. The pupa of this species measures around 5.5 to 7.5 centimeters in length, and is light brown with black spots and a black line down the middle

The stage your critter is in probably resembles Fig. 1. It's probably fine.

Fig. 1. Caterpillar just before pupating. source: wikipedia


Are mutations random? The following claim

  Mutations are random

or just the use of the expression

  Random mutations

are very common among lay people.

The claim is very common among lay people. The claim is often made by OPs (such as here, here for example) but also in answers (such as here for example).

What does it mean exactly?
Are mutations really random?

Short answer
The claim is unclear but is essentially misleading and wrong. However, IMO, for lay people, it is a good approximation to just think that mutations are random!
Here, on Understanding evolution is a great source of information on what it means to say that mutations are random
Long answer
What is a mutation?
Mutation is an event causing an alteration in the DNA sequence where the mutation occurred. There are different types of mutations, consider for example the following Single Nucleotide Polymorphism (SNP)
Original Sequence

ATTATCTG

Sequence after mutation of the 3rd nucleotide

ATGATCTG

Note that mutations can have much more drastic effects such as the duplication of a very long sequence of DNA for example.
You might want to have a look at What is the definition of a mutation? and eventually Effect of mutation on phenotype.
What can be random?
A variable can be random. So is the term mutation a variable?
IS "MUTATION" A VARIABLE
Consider first this discussion about the term house. You can measure the height of the house or the number of windows and both the height of the house and the number of windows so that both the number of windows and the house of houses are variables but house itself is not a variable.
A mutation is an event but, just like with the house, there is no obvious number associated with the term mutations. The number of mutations occurring in a reproductive event is a variable. The effect size on fitness of a mutation is a variable. So claiming that mutations are random is unclear as we don't know what property of the mutation the claim is referring to.
WHAT IS RANDOM
Fully discussing the concept of randomness will require doing quite a bit of math and philosophy. I will not attempt to do so and will intentionally make some oversimplifications here.
The concept of randomness only makes sense if we formalize a model. The outcome of flipping a coing may seem random to you but this is true only if you assume you don't know the forces at play on the coin (the movement of the thumb, the speed of the wind, etc...). A physicist would be happy to consider a coin flip being a perfectly deterministic (deterministic = not random) process.
If a process is deterministic, it means that for a given input there is a single possible output. If a process is stochastic, then there are several (potentially an infinite number) of possible outputs. Now, stochastic does not mean fair or uniformly distributed and therefore a process can be stochastic and yet we can have some predictive power on what range of values the outcome will likely take. For example a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform.
So, to talk about the claim mutations are random, ideally one would need to fully specify a model of consideration.
RANDOM AS DIRECTIONLESS
Often by random, people mean "directionless" (or "fair"). This is clearly not what the term random means but I will still discuss the case of "direction" (or "fairness") as it is often what people mean. If a mutation is directionless, it means that this mutation is not more likely to increase the value of the variable than to decrease it. For example, if the variable of interest is the height of the individual, assuming that mutations are truly directionless, a mutation is not more likely to increase the height of an individual than to reduce it.
Is the number of mutations random?
VARIATION IN MUTATION RATE
The mutation rate varies dramatically among species and along genomes roughly speaking from a rate of $10^{−2}$ to a rate of $10^{-10}$ mutation per nucleotide. For example microsatellites (repeated sequences) are highly mutable.
EFFECTS OF NEARBY SITES
Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication).
PLASTICITY FOR MUTATION RATE
The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants and bacteria typically) (Chary et al. 1993; Bjedov et al. 2003). The environment affects the mutation rate and the environment can be chosen by some species (avoidance) or even constructed by others (niche construction).
AGE OF THE PARENTS
In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. See the post Gender and age-specific mutation rate in plants (and its references) for more information.
EPIGENETICS
Epigenetic changes (do not concern all species) can also affect the mutation rate and even influence what new nucleotide the old nucleotide will be mutated into (with a given probability).
CONCLUSION
Many things affect the mutation rate. However, the exact number of new mutations an offspring will carry is not perfectly deterministic.
Type of mutations
Mutations are more likely to be transitions than transversions. But again, it is not a perfectly deterministic process.
Effect of mutations on fitness
DISTRIBUTION OF FITNESS EFFECTS
Different mutations have different effects on fitness. We talk about the Distribution of Fitness Effects (DFE).
The DFE varies from one sequence to another. In conserved sequences, mutations tend to have a higher impact on fitness.
ARE MUTATION EFFECTS ON THE FITNESS DIRECTIONLESS?
No, most mutations are deleterious or neutral. Only few mutations are beneficial.
Effect of mutations on the phenotype
Again, some phenotypes are more sensitive to new mutations than others. The increase in phenotypic variance due to mutation at every generation is called the mutational variance.
ARE MUTATION EFFECTS ON THE PHENOTYPE DIRECTIONLESS?
It can be the case, but it is not necessarily true. When mutations are not directionless, we talk about mutation bias (see for example Eyre-Walker 1998, Harr and Schloterrer 2000 or Shah et al. 2010).
Conclusion
Yes, there is some randomness in many of the variables associated with mutation events. However, it would be wrong to think that we have no predictive abilities in the number of mutations or effect of mutations, it would be wrong to think that a mutation is as likely to increase fitness than decrease it and it could be wrong to think that a mutation is as likely to increase a phenotypic trait than decreasing it.
Related posts

Are evolutionary mutations spontaneous?
What are the major causes of mutations in DNA?

Source of information in evolutionary biology
Understanding Evolution by Uc Berkeley is a good, short and very introductory course to evolutionary biology.


205 nm UV-Vis readings Typically we determine the concentration of proteins using a 280 nm reading. However, it is reasonable to use 205 nm. I was curious about the effectiveness of this method.

This may be what you are looking for. The conversion formula is:

$$
\text{Protein concentration (mg/ml)} = \frac{ (\text{Absorbance at 205 nm})} {31}
$$

The first, Scopes, does indicate that nucleic acid contaminants will confounding 205 nm absorbance readings. It seems as though this spetrophotometic calculation is feasible for relatively pure protein species.


Do trap door spiders have 10 legs? I was reading this National Geographic article, 50 New Spiders Discovered In Australia when I became confused by the two trapdoor spider species photographed. I looked up trapdoor spiders and looking at pictures, they all seem to me to have five pairs of legs. I know spiders have eight legs; can someone tell me what am I missing here?

Ctenizidae:

Euoplus:

Cork lid:

(OK, so I found out that the things next to the mandibles are pedipalps. How are they different from legs on these beasts?)

The definition of a leg from Merriam-Webster is

  "One of the rather generalized segmental appendages of an arthropod used in walking and crawling"

As Gerardo Furtado has already stated, the front pair of appendages are called palpi and are not used for walking, but for mating and manipulating objects. By this definition, palpi are not legs and therefore trap door spiders have 8 legs, not 10. More information on the rather large pali found on trap door spiders can be found in P.D. Hillyard's The Private Life of Spiders.

Image from Biodiversityexplorer.org.


Why is AMR not widespread? we know that resistant strains (MDR, XDR, PDR) have arisen in single incidents around the globe but why are these bacteria not common and not spreading quickly as humans keep using antibiotics and killing the non-resistant strains which these Amr strains have to compete for resources. One might say that they ARE spreading but my question is why is the increase in population so slow. compare it with malaria parasite 'plasmodium' which despite being a higher organism with slower reproduction cycle kills so many.

Natural selection is environment-dependent. A mutation that makes an individual more fit in one context, might make it less fit in a different context.

The mutations that make bacteria more fit in an environment where they're exposed to antibiotics generally make them less fit in a "natural" environment where they don't have to deal with antibiotics. That means that MDR bacteria are often out-competed by their less-resistant competitors, unless they're in the "right" environment for them, such as a hospital or an infected, antibiotic-treated patient.

Some references:

Barnett M, Busby SR, Mitchison DA. Tubercle bacilli resistant to isoniazid: virulence and response to treatment with isoniazid in guinea-pigs and mice. Br J Exp Pathol 1953; 34:568–81.
urgos M, Deriemer K, Small PM, Hopewell PC, Daley CL. Effect of drug resistance on the generation of secondary cases of tuberculosis. J Infect Dis 2003; 118:1878–84.
Davies AP, Billington OJ, Bannister BA, Weir WR, McHugh TD, Gillespie SH. Comparison of fitness of two isolates of Mycobacterium tuberculosis, one of which had developed multi-drug resistance during the course of treatment. J Infect 2000; 41:184–7.
Gagneux S, Long CD, Small PM, Van T, Schoolnik GK, Bohannan BJM. The competitive cost of antibiotic resistance in Mycobacterium tuberculosis. Science 2006; 312:1944–6.
Li Z, Kelley C, Collins F, Rouse D, Morris S. Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs. J Infect Dis 1998; 177:1030–5.
Middlebrook G, Cohn M. Some observations on the pathogenicity of isoniazid-resistant variants of tubercle bacilli author. Science 1953; 118:297–9.
van Soolingen D, Borgdorff MW, de Haas PE et al. Molecular epidemiology of tuberculosis in the Netherlands: a nationwide study from 1993 through 1997. J Infect Dis 1999; 180:726–36.


Why don't we form immunity to some infections? I read another question, and its answers, about how vaccines work, but I don't see there, and and don't understand, why some infections can, seemingly, not be immunized against at all. For example, someone who gets the flu (or the flu vaccine) is immunized against that particular strain of flu for life (which was relevant, IIRC, when H1N1 came back a few years ago: many people above a certain age had immunity), whereas one person can get group-Α strep throat over and over again. Why is this?

The answer is sort of hidden behind the very first paragraph of your linked question:

  Vaccines work by introducing an attenuated strain of the pathogen (or alternatively the antigens that are normally present on the pathogens surface) into the body, whereupon the body mounts an immune response.

The body mounts an immune response based upon a particular epitope (molecule/protein chain) derived from the infection itself.

If the bacteria/virus/parasite evolves so that the molecules/proteins on its surface change significantly, then the version stored in Memory Cells will no longer apply. There's some wiggle room depending on epitope length and specificity of the Immune Response (highly specific MHC proteins will invoke a very strong, very efficient response - while less specific [usually B-cell or early T-cell responses] will invoke a weaker, less effective response), but because pathogens can mutate so quickly it's not uncommon that you'll encounter a descendant of a virus you already encountered that has dramatically different characteristics.

Some pathogens are also just very "clever" at avoiding the immune system. Sometimes they can produce shells which can't be broken down to derive epitopes from, sometimes they live within host cells and simply hide (the most well known example being HIV), other times they can present the same "I'm part of the body!" MHC proteins that tells the immune system not to attack them, and they can even hide in parts of the body where the immune system rarely visits (eyes, brain, other very specialized tissues).

And at times the pathogen can be both very adaptive and very "clever", as in the case for Staphylococcus aureas - which can inactivate antibodies through surface proteins and has the ability to adapt to new antibodies very quickly.

You can think of it like a game of chess. If you play against the same person all the time you're going to learn their moves, their strategy, and be able to beat them very quickly. If you switch partners, or your regular partner learns new moves, you'll spend some time adapting to the new play style you've encountered before being able to win consistently again. Bacteria and virii are simply very, very good at coming up with new play styles.


Free-flowing cells and those that are stuck together? I've been thinking about the development of an embryo from the zygote stage.

How is it that when cytokinesis takes place at that stage, the cells all stick together in a little ball, but later in life, some are not bound to others (red blood cells, sperm cells, etc.)?

In other words, how is it that some cells are stuck together and some are separated? How does this property develop?

Cell-cell adhesion is a well-regulated mechanism, cells don't just stick together randomly, this interaction is mediated by specific molecules on the cell surfaces. The responsible proteins for that are the Cell Adhesion Molecules (CAMs) like integrins, cadherins and selectins. Which of these CAMs are present on the surface of a cell determines if those cells will bind to each other or not.

Cells can change their ability to adhere to each other or the extracellular matrix by expressing or not expressing different kinds of these molecules.

You can find a lot more information about this topic in the cell-cell adhesion chapter of "Molecular Biology of the Cell", available on the NCBI homepage.


How do biologists quantify "gene expression" in experiments? I've read papers which contain statements such as "control of gene expression is critical in biological processes".

How exactly does one quantify "gene expression"? Isn't gene expression an umbrella term describing all of the mechanism by which DNA is synthesized into an organism's phenotype?

The primary product of protein coding genes are mRNAs.  When we talk about measuring gene expression we want to assay the steady-state levels of a specific mRNA within a cell.  This is usually accomplished by starting with a large number of cells and harvesting all of the mRNAs from all of the cells.  One way to measure the expression level of just one gene's mRNA is to perform a Northern Blot.  Other sensitive methods include: an S1 nuclease protection assay, an RNAse protection assay, and a primer extension assay.

Microarrays have also been used extensively to measure expression levels of thousands of genes at the same time in a single experiment.

With the advent of RNA-Seq methodology it is possible to count the number of transcripts in an experiment (if you have a sequenced reference genome)


Why some traits are more desirable in the sexual selection? For example, why do peacock females choose males with the biggest tail? If there is no advantage in such tail.

There are two common explanations both are difficult to demonstrate. I personally favor the former but I will not claim it is the only explanation.

selection starts as either a random occurrence or as some initially beneficial trait (a slight increase in tail length may have been beneficial originally)
Then runaway selection takes over. Any increase also causes increased attraction because the evolved behavior of the desire in the females only functions as bigger is more attractive(or whatever=more attractive). This pushes further and further into absurdity becasue there is not behavioral regulation to say enough is enough. So any increase in the males increases attractiveness meaning any individual male with less can't reproduce in the current population of females no matter how beneficial to the individual male survival. Additionally no female will develop a favoring of smaller tail feathers becasue her smaller tailed offspring will not be able to find mates for the same reason. A positive feedback loop like this won't stop until it hits a point where the cost of tailfeather is more than the advantage of increased mating becasue the individual never lives long enough to mate.
By carrying a handicap the organisms shows it can withstand a greater burden and thus must be better.


Would oxygen levels be stable without photosynthesis? I learned how the CO$_2$ cycle works in several biology classes, high school, elementary school, geology, and physics. Then today there was an article published in the NY Times claiming:

  ...it is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere's oxygen content would change by less than 1 percent.

I'm really confused. If the earth naturally has 20% oxygen in the absence of photosynthisis, why did it spike durring Great Oxygenation Event? I reread that several times. There's no citation; no further context that can explain this. If this were coming from the climate change denier camp, I'd just shrug it off, but the credentials would say otherwise. It's in the NY Times and Nadine Unger is an atmospheric chemist at Yale.

My guess is that this is simply a misleading paragraph with a grain of truth. The question is, where is that grain? How long would the atmospheric oxygen content remain at within 1% of the current level if we turned off photosynthesis?

The answer to your question is in the first graph of the Wikipedia article you linked to: Great Oxygenation Event. In that graph, where time is measures in billions of years, you see that O2, as it was produced, was absorbed in oceans, seabed rock, land surfaces, and finally, about .85 billion years ago, O2 sinks filled and the gas accumulated in the atmosphere.[1] The spike you speak of was probably due to

  the evolution of the large vascular land plants that brought about increased O2 production and increased O2 levels due to the enhanced global burial of microbially resistant, lignin-rich organic matter during the Permo–Carboniferous (Berner 2004).

More simply put, there hadn't been equilibrium established yet between the amount of oxygen being produced, the stabilization of the ocean layers and the 'burial of excess carbon' in the deepest ocean layers. Most of the O2 on earth was produced many millions of years ago; it is a myth that the O2 we breathe today is the same O2 made by, say, ocean phytoplankton yesterday.

Nadene Unger states in the NYT article that

  [I]t is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere’s oxygen content would change by less than 1 percent.

This is because there are tremendous oxygen sinks that store oxygen gas, such as the surface layers of the ocean. As O2 is used, the ocean would give up free O2. Because of these sinks, some estimate that

  if photosynthesis were to cease, atmospheric oxygen would be depleted in 5000 years due to respiration, weathering, and combustion.[2]

while others state that

  If photosynthesis were for some reason to stop, oxidation of the entire organic carbon reservoir would consume less than 1% of O2 presently in the atmosphere and there would be no further O2 loss (since there would be no organic carbon left to be oxidized). Conversely, if respiration and decay were to stop, conversion of all atmospheric CO2 to O2 by photosynthesis would increase O2 levels by only 0.2%.[3]

It is very hard to get a comprehensive answer of what would happen exactly. Do we assume all vegetation/phytoplankton suddenly disappears, or does it die (thus increasing to the carbon drain on O2)? Do we assume quick quick death of animals based on lack of vegetation/plankton, etc. as food, or would it be slower? As I said, a comprehensive answer is difficult to find. In any case, the atmospheric O2 would not fluctuate wildly in any immediate fashion.

[1] The oxygenation of the atmosphere and oceans Heinrich D Holland, Phil. Trans. R. Soc., 29 June 2006
[2] The Global Oxygen Cycle
[3] Introduction to Atmospheric Chemistry


What's the duration between the binding of adrenaline to β-AR and the first translated protein? Binding of adrenaline (epinephrine) to the β-Adrenergic receptor leads to formation of cAMP (via G protein activation), activation of protein kinase A and subsequently to the expression of specific genes related to glucose metabolism.

How long does it take (in units of time) until translation of the first protein related to the adrenalin binding event is completed?

EDIT: I can accept a reasonable guess at the time scale (+/- factor of ten). Also, it can be also any another kind of ligand/receptor system.

Things can certainly vary for different ligands and different levels of cascading but these are the reactions that you may consider.

Receptor activation
Nuclear translocation (lets assume it is just a part of the receptor. You can assume secondary messengers; it will add an extra step)
DNA-binding and Transcription activation
Transcription
Nuclear export of mRNA
Translation

Finally I guess what you really want is to know when steady state is reached. This will also depend on other factors such as:

Receptor deactivation rate
mRNA and protein degradation rates
Nuclear export of activated TF
Network architecture (some networks can speed up response times). This factor can be ignored and we can consider an open loop.

Phosphorylation reactions are generally much faster than transcription/translation/translocation rates and can also assumed to be equilibrium with dephosphorylation reactions.

Nuclear import rates are also dependent on cell volumes and for polarized cells like neurons it will be much higher. The average import rate is around 0.2 - 1.2 s-1 NPC-1 µM-1(cargo) [where NPC is number of Nuclear pore complexes which is again on an average 120 ] [1].
It can be, for ease, assumed to be ~0.02 min-1 [2].

In most modeling papers the transcription rate is assumed (based on experimental reports) to be 1 per min (Average polymerase speed of ~1000nt/min and gene length of 1000nt. This can vary with gene length)

Translation rates are somewhat trickier. The translation rate per ribosome translation elongation rate is ~5 codons/sec (15aa/sec)[3] or perhaps may even be lower — 3 - 9aa/s[4] ( [3] is a more recent finding). However, the overall translation rate will be dependent on number of ribosomes (Ribosomes can be assumed to be infinite unless it is some condition like stress or starvation. By no of ribosomes I meant polysomes per mRNA, which can also vary). Also, the protein synthesis rate will depend on length of mRNA. This is one parameter that can have a broad range of values (0.6-100 min-1 × mRNA).

You can set up mathematical model (based on reaction rate equations) and calculate the response times (Depending on parameters it can be 8-20 hours). Steady states can generally reach by 8 hours (based on my own experiment. But I used tetracycline to induce luciferase). Another experiment (unpublished) using IFNγ induction caused a peak in the reporter at ~12h. I am not linking all references (you can easily look up for these). Usually, for cell culture applications, there is some sort of unsaid rule to assume 12h as a general response time to persistent stimuli. Response times are also dependent on initial conditions.

Note: Response time means the time required to achieve steady state. This does not mean the delay between signal onset and protein synthesis. Other metric that is used generally is max-peaking time.